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O'Neill, Mark. "Cardiovascular regulation under physiological stress." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294358.
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Tur, Jared. "Cardiovascular regulation by Kvβ1.1 subunit". Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6596.
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Heterologous expression systems such as COS-7 cells have demonstrated the profound effects of KCNAB1-3 or Kvβ1-3 proteins on voltage gated potassium channels (Kv) channels. Indeed, in the presence of these β-subunits transiently expressed Kv channels are often modulated in multiple ways. Kv channel membrane expression is often increased in the presence of β-subunits. In addition, non-inactivating Kv currents suddenly become fast-inactivating and fast-inactivating channels become even faster. While much research has demonstrated the profound effects the β-subunits in particular the Kvβ1 subunit have on transiently expressed Kv currents little to date is known of the physiological role it may play. One study demonstrated that by “knocking out” Kvβ1 cardiomyocyte current changes were noted including a decrease in the Ito,f current. While this novel finding demonstrated a key cardiac physiological role of the Kvβ1 subunit it left many unanswered questions as to determine the cardiovascular regulation the Kvβ1 subunit provides. Indeed, cardiac arrhythmias and other electrical abnormalities within the heart such as long QT present patients with many unfortunate unknowns. Many of these incidences occur often abruptly with cardiac electrical abnormalities. Genetic research has begun to shine light on key cardiovascular genes in particular those coding for ion channels and auxiliary subunits or β-subunits. Kv channels and their β-subunits have gained particular notoriety in their key responsibility in restoring the resting membrane potential known as the repolarization phase. Indeed genetic manipulation and physiological examination of Kv channels and recently their β-subunits has demonstrated profound physiological results including prolonged QT durations within mice altered functional activity during physiological cycles such as estrus. While initial findings of Kvβ1 have demonstrated profound cellular and cardiomyocyte current alterations much still remains unknown. Therefore, this work hypothesizes that the Kvβ1 subunit provides a profound cardiovascular role in regulation and redox sensing at the physiological and pathophysiological level in both males and females. This work identifies a sex-based difference in cardiovascular regulation by Kvβ1 as well as demonstrated a profound redox sensing ability during altered metabolic states seen in pathophysiological conditions.
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Ylitalo, A. (Antti). "Cardiovascular autonomic regulation in systemic hypertension." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:9514252128.
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Abstract
Neurogenic factors are known to be important in the development of hypertension. Our current knowledge of the role of autonomic nervous system in chronic hypertension is, however, limited. The purpose of the present study was to evaluate the possible abnormalities in heart rate variability (HRV) and baroreflex sensitivity (BRS) in patients with long standing systemic hypertension compared to subjects without evidence of cardiovascular disease. A particular aim was also to examine whether genetic variation in the renin-angiotensin-aldosterone system (RAS) genes have an influence on cardiovascular autonomic regulation.
Case-control studies were carried out on a total of 280 normotensive and 214 hypertensive subjects drawn from a random middle-aged population originally recruited for an epidemiologic study of cardiovascular risk factors. The possible association of BRS with the genetic polymorphisms of renin-angiotensin-aldosterone system genes was studied in a cross-sectional study of 315 healthy controls. Genetic associations were also tested in a younger, independent population sample of 66 subjects. The effects of intensified antihypertensive treatment on autonomic cardiovascular control were evaluated in 33 hypertensive patients with poor blood pressure control.
Wide interindividual variation in both HRV and BRS was observed in normotensive as well as hypertensive subjects. Overall HRV and autonomic responses to a change in body posture were blunted in long-standing hypertension. Decreased HRV was mainly related to elevated blood pressure and obesity.
For the first time in a population-based study, it was confirmed that BRS is impaired in patients with long-standing hypertension despite adequate antihypertensive treatment. In contrast to HRV, BRS was reduced in hypertensive subjects also after adjustment for blood pressure and obesity. BRS also varied widely both between healthy and hypertensive individuals. The wide interindividual variation in the markers of autonomic cardiovascular regulation was not, however, completely explained by demographic variables, cardiovascular risk factors or lifestyle, suggesting a genetic component contributing to HRV and BRS.
The polymorphism in the aldosterone synthase (CYP11B2) gene was found to strongly associate with BRS in two independent random populations of apparently healthy subjects. The association was even stronger in the younger population. On the basis of the observations made in the older population, it seems possible that women are protected against the effect of age and blood pressure on BRS and tend to maintain the genomic influence longer.
Intensified antihypertensive combination therapy improved blood pressure control and caused regression of left ventricular hypertrophy, and resulted in significant improvements of HRV and BRS.
The present study shows that HRV and BRS are altered in long-standing systemic hypertension. Together with age, blood pressure and obesity, genetic factors seem to be important determinants of BRS. However, abnormal autonomic cardiovascular regulation does not seem to be an irreversible phenomenon, but can be partly restored by modern combination antihypertensive therapy.
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Maa, Ming-Hokng 1977. "Alterations in cardiovascular regulation and function assessed using cardiovascular system identification." Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/86525.
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Thesis (S.B. and M.Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2000.<br>Includes bibliographical references (p. 65-67).<br>by Ming-Hokng Maa.<br>S.B.and M.Eng.
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Piira, O. P. (Olli-Pekka). "Effects of emotional excitement on cardiovascular regulation." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526209708.
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Abstract The incidence of adverse cardiovascular events is higher among spectators of exciting sports events, particularly in patients with coronary artery disease (CAD), but the mechanistic link between the events is not known. We assessed the hemodynamic, autonomic function, plasma catecholamines, endothelin-1, interleukin-6, and markers of platelet activation and blood coagulation of enthusiastic male ice hockey spectators with CAD (n=55, 60±9 years) and healthy subjects (n=16, 48±6 years) during Finnish national league ice hockey final play-off matches and on a control day. Blood markers were also measured before and after a maximal exercise test with a bicycle ergometer. Systolic and diastolic blood pressure (BP) were significantly higher one hour before, during, and one hour after the match than on the control day. During the match the highest systolic BP was 180±14 vs. 145±15 and diastolic BP was 103±13 vs. 82±11 mmHg (respectively, p<0.001 for both). Heart rate (HR) was higher throughout the match (p<0.05) and remained elevated two hours after the match (p<0001), and measures of HR variability were decreased during the match (p<0.01). Plasma endothelin-1 (ET-1), interleukin-6 (IL-6) and noradrenaline (NOR) increased during the match (p<0.01 for all), but markers of platelet activation and coagulation remained unchanged. ET-1 did not change during exercise but NOR, adrenaline, IL-6, and markers of platelet activation and blood coagulation increased statistically significantly (p<0.0001 for all). A statistically significantly more marked increase in both endothelin-1 and interleukin-6 was observed in CAD patients compared with healthy subjects during the match (time x group interaction p<0.05 for both). The high-frequency power of R-peak-to-R-peak intervals decreased in CAD patients (p<0.001) but did not change in healthy subjects during the match. Maximal metabolic equivalens (METs) were most strongly correlated with ET-1 response during the match (β =-0.45, partial correlation r=-0.43, p=0.002) when age, body mass index, METs, left ventricular ejection fraction, basal ET-1 and subjective experience of excitement were entered into the model as independent variables in a linear stepwise regression analysis. In conclusion, autonomic reactions and vasoconstriction may partly explain the vulnerability to cardiovascular events caused by this type of leisure-time emotional excitement. Emotional excitement causes concomitant increases in markers reflecting vulnerability to atherosclerotic plaque complications, while physical exercise causes more prominent changes in markers of coagulation. Emotional excitement causes more significant increases of markers of vasoconstriction and acute inflammation and withdrawal of cardiac vagal regulation in patients with CAD than in healthy subjects. Exercise capacity may protect against further cardiovascular events in CAD patients because it is associated with reduced ET-1 release during emotional excitement<br>Tiivistelmä Jännittävän urheilutapahtuman on havaittu lisäävän sydäntapahtumia erityisesti sepelvaltimotautipotilailla. Syyt eivät ole selvillä. Tutkimuksen kohteena oli jääkiekon mestaruussarjan pudotuspelien seuraamisen vaikutus sekä sepelvaltimotautisten (n=55, 60±9 vuotta) että terveiden (n=16, 48±6 vuotta) jääkiekkofanien verenkiertoon, autonomiseen hermostoon, veren katekolamiinien, endoteliini-1:n (ET-1) ja interleukiini-6:n (IL-6) pitoisuuksiin sekä veren hyytymiseen paikan päällä jäähallissa seurattuna. Muuttujat mitattiin jäähallissa ottelun aikana. Ne mitattiin myös ennen ottelua ja eri päivänä sairaalassa ennen kuntopyörällä tehtyä maksimaalista sydämen kuormitustestiä ja heti sen jälkeen. Sepelvaltimotautipotilaiden ylä- ja alaverenpaineet kohosivat tilastollisesti merkitsevästi tuntia ennen jääkiekkopeliä ja sen aikana, ja ne olivat koholla vielä tunnin ajan pelin jälkeen kontrollipäivään verrattuina. Ottelun aikana yläpaineet olivat 180±14 vs. 145±15 ja alapaineet 103±13 vs. 82±11 mmHg (p<0.001 molemmille painetasoille). Sydämen syke oli korkeampi pelin ajan (p<0.05), ja se pysyi koholla kahden tunnin ajan pelin jälkeen (p<0.001). Lisäksi sykevaihtelu heikentyi pelin aikana (p<0.01) kontrollipäivään verrattuna. Veren ET-1-, IL-6- ja noradrenaliinipitoisuudet (p<0.01) nousivat pelin aikana, mutta veren hyytymistä kuvastavat lukemat säilyivät muuttumattomina. ET-1 ei noussut fyysisessä kuormitustestissä, mutta noradrenaliini- ja adrenaliinipitoisuudet sekä IL-6:n ja veren hyytymistä kuvaavat lukemat kasvoivat tilastollisesti merkitsevästi (p<0.0001). Pelin aikana sepelvaltimotautipotilaiden ET-1 ja IL-6 pitoisuudet kohosivat enemmän kuin terveiden vastaavat arvot (p<0.05). Lisäksi ottelun aikana sydämen sykevaihtelu laski sepelvaltimopotilailla (p<0.001), muttei muuttunut terveillä. Polkupyörätestin maksimaalinen suorituskyky (METs) oli voimakkaasti yhteydessä ET-1 vasteeseen pelin aikana (β =-0.45, r=-0.43, p=0.002), kun ikä, painoindeksi, METs, sydämen supistusvireys, ET-1:n lähtötaso ja koehenkilöiden kokema jännitystaso huomioitiin itsenäisinä muuttujina regressiotyyppisessä tilastolaskennassa. Yhteenvetona todetaan itsenäisesti toimivan hermoston muutosten ja verisuonten supistumisen voivan osittain selittää aiemmin havaitun sydäntapahtumien lisääntymisen tutkimuskohteen tyyppisessä vapaa-ajan tunne-elämyksessä. Jääkiekkopelin jännitys aiheuttaa muutoksia sepelvaltimotautialueiden repeämisherkkyyttä kuvaaviin tekijöihin, kun taas fyysinen rasitus vaikuttaa voimakkaammin veren hyytymistä ilmaiseviin lukemiin. Potilailla jännitys lisäsi enemmän suonten supistuvuutta, akuuttia tulehdusreaktiota ja nosti parasympaattisen hermoston vetäytymistä kuvaavia lukemia terveisiin koehenkilöihin verrattuna. Hyvä suorituskyky voi suojata korkean riskin sepelvaltimotautipotilaita sydäntapahtumilta vähentämällä ET-1:n vapautumista jännityksen aikana
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DeGrande, Sean Thomas. "Phosphatase regulation in cardiovascular physiology and disease." University of Iowa, 2012. http://ir.uiowa.edu/etd/3443.
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Reversible protein phosphorylation is an essential component of metazoan signaling and cardiovascular physiology. Protein kinase activity is required for regulation of cardiac ion channel and membrane receptor function, metabolism, and transcription, and aberrant kinase function is widely observed across disparate cardiac pathologies. In fact, multiple generations of cardiac therapies (eg. beta-adrenergic receptor blockers) have targeted cardiac kinase regulatory cascades. In contrast, essentially nothing is known regarding the mechanisms that regulate cardiac phosphatase activity at baseline or in cardiovascular disease.
Protein phosphatase 2A (PP2A) is a key phosphatase with multiple roles in cardiac physiology. Here we demonstrate the surprisingly complex regulatory platforms that control PP2A holoenzyme activity in heart. We present the first full characterization of the expression and regulation of the PP2A family of polypeptides in heart. We identify the expression of seventeen different PP2A genes in human heart and define their differential expression and distribution across species and in different cardiac chambers. We show unique subcellular distributions of PP2A regulatory subunits in myocytes, strongly implicating the regulatory subunit in conferring PP2A target specificity in vivo. We report striking differential regulation of PP2A scaffolding, regulatory, and catalytic subunit expression in multiple models of cardiovascular disease as well as in human heart failure samples. Importantly, we demonstrate that PP2A regulation in disease extends far beyond expression and subcellular location, by identifying and describing differential post-translational modifications of the PP2A holoenzyme in human heart failure. Furthermore, we go to characterize a mechanism for this method of post-translational modification that may represent a pathway capable of being therapeutically manipulated in human heart failure. Lastly we provide evidence that dysregulation of phosphatase activity contributes to the cellular pathology associated with a previously described inheritable human arrhythmia syndrome, highlighting the importance of the PP2A in cardiovascular physiology and disease. Together, our findings provide new insight into the functional complexity of PP2A expression, activity, and regulation in heart and in human cardiovascular disease and identify potentially new and specific gene and subcellular targets for the treatment of human arrhythmia and heart failure.
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Keramatipour, Mohammad. "Regulation of cardiovascular cell phenotype by BTEB3." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616239.
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Way, Monica A. "Regulation of cardiovascular responses from the infralimbic cortex." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq28684.pdf.
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Ferro, Albert. "#beta#-adrenoceptor cross-regulation in the human cardiovascular system." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318286.
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Mcginley, Jared Joseph. "Lateralized Induction of Cardiovascular Responses: Exploring Asymmetric Autonomic Regulation." Thesis, Virginia Tech, 2012. http://hdl.handle.net/10919/32888.
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There is clear evidence that the autonomic nervous system (ANS) is lateralized at both the peripheral as well as the central levels of the nervous system. Both the vagus and the sympathetic ganglia asymmetrically innervate the sino-atrial node and the myocardium of the heart. This lateralization has also been observed in afferent as well as efferent projections to nuclei in the brainstem, hypothalamus, and amygdala. Where laterality has not been as clear is in regions of the frontal lobe dedicated to the regulation of autonomic nervous system responses. This study addressed that issue via the implementation of lateralized autonomic response-evoking tasks. With the use of cardiovascular and electrodermal measures, the present study indexed autonomic responses to lateralized stimuli. This study also explored the role of lateralization within sex as well as in relation to reported gender identity. The findings lend support to the right hemisphere as serving a dominant role in regulating sympathetic nervous system activity, while lending less conclusive support for lateralization of parasympathetic nervous system regulation. Men demonstrated greater lateralization for sympathetic nervous system responses across several different metrics of autonomic indices. The exploration of gender variables in relation to lateralization of autonomic responses was generally not supported.<br>Master of Science
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Rees, Daryl David. "The role of nitric oxide in the cardiovascular system." Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293301.
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Nitric oxide is generated by the vascular endothelium from L-arginine by a constitutive, Ca2+-dependent, NO synthase. Analogues of L-arginine were characterised as inhibitors of NO synthase to investigate the biological significance of the L-arginine-NO pathway in the vessel wall and its role in the cardiovascular system. These inhibitors attenuate the endothelium-dependent vasorelaxation and hypotension induced by various agents, produce an increase in vascular tone and an increase in blood pressure. This suggests that NO is involved in endothelium-dependent relaxation and its continuous release maintains a vasodilator tone and plays a fundamental role in the regulation of blood flow and blood pressure. The removal of the NO-dependent vasodilator tone, results in an `upregulation' of its intracellular receptor, the soluble guanylate cyclase and an increased sensitivity to those vasodilators which act by stimulating this enzyme. This phenomenon of `supersensitivity' to nitrovasodilators may be an important component of their therapeutic action in certain cardiovasulcar disorders. Vascular tissue also expresses an inducible, Ca2+-independent, NO-synthase after activation by lipopolysaccharide (LPS) which results in the generation of large quantities of NO, predominantly from the smooth muscle layer, with a consequent loss of vascular tone and a hyporeactivity to the vasoconstrictor action of phenylephrine. Induction of NO synthase in the vasculature may therefore be responsible for the hypotension and hyporesponsiveness to pressor agents characteristic of endotoxin shock. The glucocorticoid, dexamethasone inhibits the expression of this enzyme but not its activity, which may explain why steroids are more effective at preventing rather than treating this condition. These results suggest that in the cardiovascular system, NO can be considered to have both a protective and a pathological role. The release of small amounts of NO from the constitutive, Ca2+-dependent NO synthase, acts as an adaptive mechanism whereby the vascular endothelium responds to changes in its environment and regulates blood flow and blood pressure to maintain organ perfusion. In contrast, following the induction of the Ca2+-independent NO synthase, after immunological stimulation, NO is released in large quantities from vascular tissue, which may result in pathological vasodilation and tissue damage.
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曾紹怡 and Siu-yee Patricia Tsang. "Regulation of cholesterol metabolism in hepatocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969835.
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Tsang, Siu-yee Patricia. "Regulation of cholesterol metabolism in hepatocytes." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22032459.
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Ansakorpi, H. (Hanna). "Cardiovascular regulation in epilepsy with emphasis on the interictal state." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514271343.
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Epilepsy is associated with changes in autonomic cardioregulatory function. Ictally, autonomic disturbances may be evident with significant changes in heart rate (HR), blood pressure (BP) and respiration. However, interictal dysfunction of autonomic cardiovascular system may be subtle and it may be recognized only by delicate tools designed for that purpose. The aim of this study was to evaluate the function of the cardiovascular autonomic regulatory system in patients with epilepsy.
Cardiovascular reflex tests were performed on patients with partial or idiopathic generalized epilepsies. Special attention was paid to temporal lobe epilepsy (TLE). An association of refractory and well controlled TLE and hippocampal sclerosis with altered cardioregulation was evaluated by using cardiovascular reflex tests and an analysis of spectral and non-linear analysis of heart rate variation (HRV).
Cardiovascular reflexes were altered both in patients with partial and idiopathic generalized epilepsies who had been treated for epilepsy with antiepileptic drugs (AEDs), whereas patients with newly, untreated epilepsy did not differ from the control subjects. Diminished cardiovascular reflexes also seemed to be associated with carbamazepine (CBZ) treatment. Various parameters of cardiovascular reflex tests and analysis of spectral and dynamic measures of HRV were diminished in patients with TLE compared to the control subejcts.
These results indicate that epilepsy, especially TLE, is associated with interictal changes of autonomic cardioregulation. Although these changes seem to be evident in patients with severe form of TLE, patients with well controlled TLE and patients without hippocampal sclerosis also have altered autonomic cardioregulatory function. These results suggest that dysfunction of the cardioregulatory system is rather associated with functional than structural changes of the inner temporal lobe in patients with TLE.
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Claflin, Kristin Elizabeth. "The brain renin-angiotensin system in metabolic and cardiovascular regulation." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/2196.
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Leptin acts within the brain to increase resting metabolic rate (RMR) and blood pressure (BP). The renin-angiotensin system (RAS) elicits similar effects in the brain, as reviewed in chapter 1, and it has previously been shown that central angiotensin II type 1 (AT1) receptors are required for leptin-mediated inductions in sympathetic nerve activity to the brown adipose tissue. Thus, we hypothesize that the brain RAS mediates the metabolic effects of leptin. To investigate the interaction between the RAS and leptin, we generated the AT1ALepR-KO mouse which lacks the AT1A receptor in leptin-sensitive cells. In chapter 2, we demonstrated that stimulation of RMR by DOCA-salt and high fat diet requires AT1A receptors in leptin receptor-expressing cells and that these cells expressing both AT1A and the leptin receptor appear to be agouti related-peptide (AgRP) neurons. In chapter 3, we investigated the role of AT1A specifically in AgRP neurons by utilizing AT1AAgRP-KO mice. Similar to AT1ALepR-KO mice, AT1AAgRP-KO mice exhibited deficits in BAT SNA responses to leptin and induction of RMR by alpha melanocyte stimulating hormone. In chapter 4, we utilized a novel transgenic mouse model to demonstrate that microglia do not express the AT1A receptor under chow or high fat diet fed conditions. Taken together, we conclude that a subset of AgRP neurons, which express both the leptin receptor and the AT1A receptor, are critical for the control of sympathetic nerve activity and ultimately RMR.
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Padley, James. "Acetylcholine in Central Cardiorespiratory Regulation in Health and Depression." Thesis, The University of Sydney, 2007. http://hdl.handle.net/2123/10283.
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Circulation and breathing movements that are essential for life are regulated by neurons in the hypothalamus and lower brainstem. Activity of these neurons is regulated by peripheral afferent and higher order inputs that release a diverse array of amino acids, amines and peptides. In this thesis we investigated the role of the neurotransmitter acetylcholine (ACh) and its receptors in regulation of cardiorespiratory homeostasis. Secondly, we determined whether or not genetic disturbances in regulation of acetylcholine receptor sensitivity affect central control of circulation, body temperature or respiration. The findings presented in Chapter 3 reveal a novel functional role of ACh and G-protein coupled muscarinic receptor (mAChR) activation in the rostral ventrolateral medulla (RVLM). We showed for the first time that some non-C1 RVLM neurons express mRNA for the M2 or M3 receptor; however, both C1 and enkephalinergic RVLM neurons were closely apposed by c holinergic terminals positive for the vesicular acetylcholine transporter (vAChT). Physiological studies demonstrated that activation of mAChR within the RVLM in anaesthetised rats increases arterial pressure and sympathetic nerve activity and has differential effects on major cardiorespiratory reflexes: RVLM mAChR activation resets the sympathetic baroreflex to higher arterial pressures and increases its gain and, concomitantly, attenuates excitatory reflexes evoked by peripheral chemoreceptor or somatic afferent stimulation. Retrograde tracing from the RVLM combined with vAChT immunoreactivity showed that neurons in the pedunculopontine tegmental nucleus (PPT) are the sole source of cholinergic input to the RVLM. The PPT-RVLM pathway appears to be part of a central command circuit concerned with adjusting circulatory function appropriate to increased muscle activity. These data support the notion that activation of specific neurotransmitter receptors in the RVLM encodes fu nctional specificity in control of sympathetic outflow and r! eflex fu nction. The extent to which genetic variations in central mAChR sensitivity influence autonomic function is unknown. Flinders Sensitive Line (FSL) rats were bred from Sprague Dawley (SD) rats for exaggerated behavioural and hypothermic responses to cholinesterase inhibitors and direct-acting mAChR agonists. A control genetic counterpart, the Flinders Resistant Line (FRL), was also bred in parallel for reduced responses to cholinergic agonists. The findings of Chapter 5 showed for the first time that FSL rats exhibit an increase in M2 and reduction in M3 receptor expression in the rostral medulla, suggesting that cholinergic signalling in this region may be altered. However, alterations of mAChR expression specific to FSL rats were restricted to this area and there were no changes in cerebellar expression of mAChR in any strain. Physiological studies showed that conscious or anaesthetised FSL rats were more sensitive to thermoregulatory responses to central mAChR a ctivation (ie hypothermia and increase in cutaneous blood flow); whereas pressor responses were reduced compared to SD and FRL rats. The increase in sympathetic activity and depression of respiration evoked by central mAChR activation was unchanged and attenuated, respectively, in FSL rats compared to control strains. These findings indicate that mAChR involved in control of different autonomic functions are regulated independently at the genetic and / or post-transcriptional level. The findings of Chapters 4 and 6 reveal a novel effect of breeding for cholinergic hypersensitivity in FSL rats on control of vagal and sympathetic outflow. Spectral analysis of blood pressure recordings in conscious FSL rats showed a reduction in total and high frequency power of heart rate variability (HRV), an increase in the LF/HF ratio and reduction in baroreflex sensitivity (BRS) compared to controls. These changes reflect a reduction in reflex vagal input and relative predominan ce of sympathetic input to the sinus node in FSL rats. Under! urethan e anaesthesia, FSL rats had a higher heart rate and exhibited lower gain of baroreflex control of splanchnic sympathetic nerve activity (SNA). Moreover, FSL rats were more susceptible to ventricular arrhythmias during infusion of the cardiac glycoside ouabain under anaesthesia compared to controls. These data indicate that FSL rats exhibit impaired reflex regulation of vagal and sympathetic outflow that could underlie increased vulnerability to arrhythmia seen in this strain. The precise brain regions and neurotransmitters that underlie autonomic disturbances seen in FSL rats are unclear. As well as muscarinic hypersensitivity, FSL rats also exhibit increased sensitivity to nicotine, serotonin and dopamine. Multiple chemical sensitivities in FSL rats may arise from functional interactions with mAChR or changes in common intracellular regulatory or signalling pathways. FSL rats exhibit a number of behavioural and somatic abnormalities consistent with clinical depre ssion, including reduced motivated behaviour and sleep and psychomotor disturbances. These symptoms are also alleviated by treatment with antidepressants, suggesting that similar neurochemical abnormalities may underlie behavioural disturbances seen in FSL rats and human depression. Symptoms of depression are an emerging risk factor in the development of cardiovascular disease and are associated with increased risk of dying from a cardiac-related event. A reduction in HRV and BRS in depressed patients has been widely reported and is considered to be a key substrate predisposing to arrhythmia in this patient group. In this thesis we demonstrate for the first time that FSL rats exhibit similar autonomic abnormalities to those reported in human depression and are more vulnerable to ouabain-induced ventricular arrhythmias. These findings suggest that biological factors predisposing to autonomic dysfunction and arrhythmia in FSL rats could also operate in human depression. This m ay involve altered neurotransmission in cardiovascular brain! regions , or inappropriate regulation of cardiovascular function by arousal or motor control pathways. Overall, this thesis provides novel insights into cholinergic mechanisms that regulate cardiorespiratory homeostasis. ACh is important in physiological regulation of circulation via activation of G-protein coupled mAChR in the RVLM. Selective breeding for cholinergic hypersensitivity in FSL and FRL rats results in region- and subtype-specific changes in mAChR expression in the lower brainstem and differentially influences muscarinic control of circulation and breathing. Variations in central mAChR sensitivity may contribute to impaired reflex control of vagal and sympathetic outflow and could hence predispose to cardiac complications including arrhythmias. Future studies may aim to further understand the relationship between endogenous sensitivity of metabotropic neurotransmitter receptors in the CNS and cardiovascular disturbances associated with depression.
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Stenger, Michael Brian. "HUMAN CARDIOVASCULAR RESPONSES TO ARTIFICIAL GRAVITY TRAINING." UKnowledge, 2005. http://uknowledge.uky.edu/gradschool_diss/252.
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Human cardiovascular adaptations to microgravity include decreased plasma volume, exercise capacity, baroreflex function as well as decreased orthostatic tolerance upon return to a gravity environment. Several countermeasures have been proposed and tested, although currently none have been developed to prevent post-spaceflight orthostatic intolerance (OI). Artificial gravity (AG) generated by short-radius centrifugation (SRC) has been proposed as a countermeasure to OI as well as other cardiovascular alterations. Methods: Fifteen men and fourteen women underwent three weeks of daily (5 days a week) exposure to intermittent (1.0 to 2.5 Gz) artificial gravity on a 1.9m human powered centrifuge (HPC) at the NASA Ames Research Center. Half the subjects exercised (active) to power the HPC while half rode passively (passive). A combination head-up tilt (HUT) and lower body negative pressure (LBNP) test was used to determine orthostatic tolerance before and after training. Oscillatory LBNP (OLBNP) was used at seven frequencies (0.01 to 0.15 Hz) for two minutes each to assess the dynamic responses of the cardiovascular system to orthostatic stress, before and after AG training. Results: Training improved overall tolerance in the group of subjects by 13% (pandlt;0.05); men were more tolerant than were women (pandlt;0.05); and active subjects were more improved than passive subjects (pandlt;0.05). Mechanisms of improvement appear to be through decreased total peripheral resistance (TPR) and increased stroke volume after training, and increased responsiveness of TPR to fluid shifts (faster changes in TPR to changes in calfcircumference [CC] and OLBNP after training). There was no change in spontaneous baroreflex sensitivity (BRS, calculated by sequence method) or number of sequences per number of heart beats (NNS), although BRS analysis did indicate that stimulation to the cardiac baroreceptors during 1.0 Gz and 2.5 Gz centrifugation was no different than supine control and 70?? HUT, respectively. Taken together, these results suggest that AG training improved tolerance through training of local mechanisms in the peripheral vasculature, or extrinsic control of peripheral vascular resistance, rather than through changes of autonomic control of heart rate.
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Berry, Narelle Margaret, and narelle berry@unisa edu au. "Acute and long term interventions to assess the adaptability of the cardiovascular responses to orthostatic stress." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070228.123618.
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This thesis comprises of four experiments from which related but independent analyses were undertaken. The interventions employed were designed to investigate the effect of cardiovascular adaptation, both in the short and long term on the cardiovascular responses to orthostatic stress. The first study, described in Chapter 3, tested the hypothesis that the cardiovascular system (CVS) could adapt to repeated orthostatic challenges in a single session. 14 subjects were exposed to ten +75° head-up tilts (HUT) over 70 mins. Each tilt involved a 5 min supine period (SUPINE) followed by 2 min HUT (TILT). Various indices of cardiovascular function were determined non-invasively. Cardiovascular responses to HUT10 for the final 30s of SUPINE and the first 30s of TILT were compared with those of HUT1. Integrated cardiac baroreflex sensitivity (BRS) was assessed using the Valsalva Manoeuvre (VM). Results showed MAP and DBP increased in both SUPINE (MAP p=0.009, DBP p=0.002) and TILT (MAP p=0.003, DBP p=0.009) for HUT10 compared with HUT1. TPR increased during TILT only (p=0.001) during HUT10 compared with HUT1. CO and SV were decreased during SUPINE at HUT10 relative to HUT1, however, there were no differences in TILT at HUT10 for either CO or SV. There was no change in the response of BRS, HR or SBP from HUT1 to HUT10. This study indicated that 10 repetitive HUTs can elicit changes in the cardiovascular responses to orthostasis, reflected by an increased TPR. The second study, described in Chapter 4, investigated the effect of the repeated HUT protocol outlined above on the cardiovascular responses to the squat-stand test (SST). 16 subjects were randomly allocated into either a tilting group that underwent ten +75° HUTs in 70 min (TILTING) or a control group that underwent 70 min of rest (CONTROL). Before and after the 70 min of either HUT or rest, subjects performed a SST (SST1 and SST2 respectively). The same cardiovascular parameters as those used in Chapter 3 were determined during both SSTs. The final 30s of SQUAT and the first 30s of STAND (divided into three 10-sec blocks termed STAND10, STAND20 and STAND30) were compared between SST1 and SST2, results were as follows. TILTING: during the SQUAT phase of SST2, SBP, MAP, DBP and TPR were significantly elevated (p less than 0.05) and HR was significantly decreased (p=0.032) compared with SST1; at STAND10, DBP and MAP were significantly increased (p less than 0.05); at STAND20, SBP was increased (p=0.03); and, at STAND30, DBP, SBP and MAP (p less than 0.05) were increased. There were no differences observed between SST1 and SST2 in the CONTROL group. Results indicated that ten consecutive +75° HUTs can improve the CVS responses to the SST. This is predominantly due to an increase in DBP, indicative of a change in vascular resistance. The third study, outlined in Chapter 5, investigated the effect of lower limb unilateral and bilateral resistance exercise on the blood pressure (BP) and HR responses in young males. 12 normotensive, sedentary young males were divided into 2 groups; one group exercised unilaterally and the other bilaterally. Thirty seconds of resting data were collected before subjects performed 4 SETs of 10-12 reps on a seated leg press. SET 1 was performed at 50% of 10-12RM, SET 2 was performed at 75% and SET 3 and SET 4 were performed at 10- 12RM. Bilateral resistance exercise elicited greater increases in SBP than unilateral exercise at SETs 2, 3 and 4 (p less than 0.05). DBP was only greater with bilateral exercise relative to unilateral exercise at SET 2 (p=0.036). There were no differences between the groups for the HR response. This study demonstrated that the BP response to bilateral lower limb resistance exercise was significantly greater than that of unilateral exercise in young sedentary males. This information could be beneficial to many populations for whom lower BP responses to exercise would be an advantage. Following on from this, to investigate long term improvements in cardiovascular responses to orthostasis the study outlined in Chapter 6, investigated the effect of acute (10 weeks) and chronic (more than 4 years) resistance training (RT) on the cardiovascular responses to both HUT and SST. 22 young males were allocated into three groups. The UNILATERAL (N=7) and the BILATERAL (N=7) groups performed baseline testing followed by 10 weeks of lower limb RT (performed unilaterally or bilaterally), followed by repeats of the tests performed at baseline. The CONTROL group (N=8) followed the same protocol except they were asked to perform no resistance training during the 10 weeks between testing sessions. An additional 7 subjects were allocated to a CHRONIC group consisting of individuals who had been training for more than 4 years. These subjects only performed the baseline testing. Baseline testing consisted of a number of cardiovascular tests, ultrasound for vein diameter, BRS via VM, and tests for calf ejection fraction and venous elasticity. Results demonstrated that neither unilateral nor bilateral RT caused an alteration in the cardiovascular response to the HUT or SST. There were no changes in any cardiovascular variable in response to acute RT relative to the control group. The CHRONIC group had a decreased cardiovascular response to both orthostatic challenges, with a decrease in SV in response to HUT being greater in the chronic group relative to the other groups (p less than 0.05) and the TPR response to SST being significantly less than the control group (p less than 0.05). The CHRONIC group also had a smaller elastic modulus for the right leg in comparison to the other groups (p less than 0.05). Results indicate that heavy resistance exercise may cause a decreased cardiovascular response to orthostatic stress and that these decreases may be controlled by a decreased venous elasticity. Collectively, these results demonstrate that the CVS is highly adaptable to repeated orthostatic stress and the dominant underlying feature of this protective adaptation is increased vascular resistance. Following the repeated HUT the CVS is in a more protected state and has become better able to defend itself against the adverse consequences of rapidly applied hydrostatic force. However lower limb RT performed bilaterally (with large increases in BP) or unilaterally (with lower increases in BP) does not improve CVS response to orthostatic stress, in fact chronic RT (more than 4 yrs) appears to impair the CVS response to orthostasis, potentially due to decreased venous elasticity.
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McQuarrie, Emily Pamela. "Mineralocorticoids and sodium in chronic kidney disease - regulation and cardiovascular implications." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3269/.
Full textAbstract:
Chronic kidney disease is common and associated with an elevated cardiovascular risk, as well as the long-term risk of renal failure. At present, therapeutic approaches to managing chronic kidney disease (CKD) do not fully reverse these risks. This has led to study of the determinants of pathological outcomes in these patients, with the hope of further therapeutic interventions to reduce these risks. Mineralocorticoids, predominantly aldosterone, are produced by the adrenal cortex and have a vital role in maintaining sodium status and blood pressure. However, high levels of aldosterone in humans are known to produce an adverse phenotype of hypertension and a disproportionately elevated cardiovascular risk. Furthermore, in animal models of renal failure, elevated aldosterone levels stimulate renal damage, in the presence of a high sodium milieu. These laboratory findings have been translated to provide a basis for several short-term follow-up clinical trials looking at the impact of non-genomic non-natriuretic doses of mineralocorticoid receptor inhibition in patients with chronic kidney disease. These studies have shown a reduction in proteinuria, often independent of decline in blood pressure. However, there is a paucity of baseline physiological data relating to the normal regulation of mineralocorticoid synthesis and action in chronic kidney disease. The response of the adrenal cortex to renal failure is not understood. Is mineralocorticoid synthesis regulated in the usual way? Are the stimulators of mineralocorticoid production and release affected by uraemia? Is dietary sodium intake associated with steroid status and adverse outcomes in humans? The hypothesis of this thesis was that the renin-angiotensin-aldosterone system is inappropriately activated in patients with chronic kidney disease. Secondly, that high levels of mineralocorticoids are associated with adverse end-organ damage including proteinuria excretion, left ventricular hypertrophy, endothelial dysfunction, elevated pulse wave velocity and markers of renal fibrosis. Furthermore, that these deleterious effects are associated with sodium status and that an elevated dietary sodium intake is independently associated with increased renal and cardiovascular risk. In order to test these hypotheses, 70 patients with CKD and 30 patients with essential hypertension (EH) were recruited and underwent detailed clinical and biochemical phenotyping. This included 24 hour urinary steroid metabolite analysis, plasma renin and aldosterone measurement, cardiac magnetic resonance imaging, carotid-femoral pulse wave velocity and assessment of endothelial function. 20 It was shown that levels of the main mineralocorticoids (MC) (aldosterone and deoxycorticosterone) are not elevated in patients with CKD, as compared with patients with essential hypertension (EH). However, the determinants of levels of MC excretion differed between the two conditions. In CKD, excretion of MC metabolites was directly proportional to excretion of urinary sodium. A high urinary sodium (a marker of dietary sodium intake) was associated with a higher excretion of tetrahydroaldosterone (THALDO - the main aldosterone metabolite). In patients with EH, no relationship was seen between urinary steroid excretion and urinary sodium excretion. This is a novel relationship between the kidney and adrenal gland which questions the conventional wisdom that the adrenal cortex is unaffected by uraemia and prompts further study into the regulation of steroid synthesis in CKD. Furthermore, it was shown for the first time that 24h excretion of tetrahydrodeoxycorticosterone (THDOC) is an independent predictor of left ventricular mass index and that THALDO is an independent predictor of proteinuria excretion – demonstrating a relationship between mineralocorticoids and two of the main predictors of mortality in CKD. An interaction between sodium, MCs and these two features was also demonstrated. No association between levels of mineralocorticoids and vascular function was seen. Urinary 24 hour excretion of sodium was significantly associated with endothelial dysfunction in patients with CKD and pulse wave velocity in patients with essential hypertension. Retrospective data analysis further confirmed an association between a high dietary sodium intake and adverse outcomes. In a study of 498 patients with CKD and a median follow-up of 7 years, an elevated 24h urinary sodium to creatinine ratio was shown to be associated with an increased risk of death. There was however no independent association with renal progression or requirement for renal replacement therapy. This is the first time that sodium intake has been clearly linked to adverse outcomes in patients with CKD. Lastly, laboratory work demonstrated that steroid stimulation (aldosterone or cortisol) of human proximal tubular cells resulted in increased collagen 1 gene expression, but only in the context of a high sodium environment. Collagen 1 is deposited in renal interstitial fibrosis. This effect was inhibited by MR blockade, further expanding on the potential role 21 of steroids in the progression of CKD and again confirming the relationship between salt and steroids. In conclusion, in this thesis it has been demonstrated that production of MCs in patients with CKD is closely associated with urinary sodium excretion (a surrogate for dietary sodium intake). This relationship is novel and not seen in patients with essential hypertension. It suggests that the response of the adrenal cortex in the context of uraemia is altered. Moreover, levels of mineralocorticoids are independently associated with left ventricular mass index and proteinuria excretion, both significant predictors of mortality, in patients with CKD. Dietary sodium intake has been shown to be an independent predictor of mortality and laboratory studies have demonstrated that mineralocorticoid receptor binding in a high sodium environment is associated with collagen 1 gene upreguation. These findings have important implications for the role of adequate renin-angiotensin-aldosterone blockade in patients with CKD and suggest that the addition of a mineralocorticoid receptor blocker and dietary sodium restriction should be advocated.
20
Moore, C. "The role of neuronal nicotinic acetylcholine receptors in central cardiovascular regulation." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444883/.
Full textAbstract:
The central effect of nicotine on cardiovascular regulation has been extensively studied. However, due to its unselective nature for nicotinic acetylcholine receptors (nAChR) the involvement of specific nAChRs at sites in the brain, in central nervous cardiovascular regulation remains unclear. The effects of intracerebroventricular (i.c.v.) and intracisternal (i.e.) injections of the a7 selective agonist, PSAB-OFP, and the a4p2 selective agonist, TC-2559, were investigated on blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) compared with nicotine, in the anaesthetised rats. PSAB-OFP and TC-2559 i.c.v. caused a delayed dose-related increase in BP and RSNA. When given i.e. the action was similar except the rise in BP was more immediate. The possibility that the pressor response was partly due to the agonists causing the release of the vasoconstrictor vasopressin into the circulation was tested by repeating the i.c.v. and i.e. injections of the agonists in the presence of a selective vasopressin Via antagonist. In the presence of Vi antagonist (i.v.), PSAB-OFP and TC-2559 (i.c.v.) now induced no change in BP or RSNA however i.e., the increase in BP and RSNA was delayed with TC-2559, while PSAB-OFP caused a decrease in BP and no change in RSNA. The cardiovascular effects of i.c.v. PSAB-OFP and TC-2559 in the presence of Vi receptor antagonist (i.c.v.) were also completely blocked. PSAB-OFP and TC-2559 (i.e.) in rats pre-treated with Vi antagonist (i.e.), no longer produced an increase in BP and RSNA. However, the delayed fall in BP caused by PSAB-OFP was potentiated. Nicotine i.c.v. caused a dose-related increase in BP and renal sympathoinhibition while i.e. the rise in BP was larger and now associated with a bradycardia. In the presence of Vj antagonist (i.v.), nicotine's (i.c.v.) cardiovascular effects were blocked however nicotine i.e. caused a decrease in BP, RSNA and HR. In the presence of Vi antagonist (i.c.v.), nicotine caused no change in RSNA, but BP still increased. In the presence of Vi antagonist (i.e.), nicotine i.e. induced a decrease in RSNA and HR, with no change in BP. This study indicates that activation of a4p2 and <x7 nAChRs in the hindbrain cause an increase in BP due to vasopressin release into the periphery, which is mediated by a central vasopressinergic pathway, possibly involving a pathway from the hindbrain to the PVN. Interestingly, the renal sympathoexcitation was also prevented by blocking Via receptors in the periphery as well as in the brain. A possible mechanism is discussed whereby vasopressin or its antagonist accesses the brain via the circumventricular organs and then indirectly influence the PVN, supra-medulla or supra-spinal vasopressin neurons influencing the renal sympathetic outflow. Nicotine also causes an increase in BP by vasopressin release into the periphery, by acting on nAChR in the forebrain and the hindbrain. Interestingly, the decrease in RSNA is still observed when in the presence of Vj antagonist, suggesting that the decrease in RSNA is partly mediated by an action of nicotine on nAChRs at sites in the hindbrain such as the NTS.
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Beck, Allison Leigh. "Hostility and Cardiovascular Regulation: An Investigation of Lateralized Pre-Motor Functions." Thesis, Virginia Tech, 2003. http://hdl.handle.net/10919/79678.
Full textAbstract:
Behavioral and physiological correlates of hostility, such as cardiovascular lability and increased risk of cardiovascular disease, are vital when considering the possible health risks associated with high levels of hostility (Henry & Meehan, 1981; Matthew & Haynes, 1986; Johnson, 1990; Heller, 1993; Heilman, Bowers, & Valenstein, 1993; Demaree & Harrison, 1997; Demaree Harrison, & Rhodes, 2000; and Shenal & Harrison, 2001). By examining this issue through a functional cerebral systems approach, one is better able to conceptualize changes that occur when men with extreme hostility levels (e.g. high and low) carry out emotional regulation tasks. High and low hostile groups have been shown to differ in their auditory, visual, somatosensory, and motor processes. Moreover, they differ in lateralized cerebral functions within these modalities where high hostiles have shown a right cerebral/ negative affective bias while low hostiles have shown a left cerebral/ positive affective bias in perception and in motor functions to stress. Right cerebral activation in high hostiles has occurred with heightened reactivity and persistence in sympathetic tone and with cardiovascular changes in heart rate, blood pressure, and Galvanic skin response. In the present experiment, this systematic line of research (Harrison & Gorelczenko, 1990; Herridge & Harrison. 1996; Demaree & Harrison, 1997; Herridge, Harrison, & Demaree, 1997; Demaree, Higgins, Williamson, and Harrison, 2002; Williamson & Harrison, in press) was extended to the investigation of the premotor frontal eye fields using rapid directional eye movements toward the contralateral hemisphere. It was predicted that high hostiles would evidence right frontal deficits in lateral eye movements (LEM) resulting in decreased LEM toward and within the left hemispace. Moreover, concurrent processing of lateralized eye movements and regulation over cardiovascular responding was predicted to yield sympathetic dysregulation on leftward LEM (lLEM) and potentially parasympathetic dysregulation on rightward LEM (rLEM). Leftward LEM appeared to result in more fatigue effects than rightward LEM. However, the primary behavioral hypothesis was not supported. Moreover, the directional relationship predicted between left side LEM and sympathetic tone was not found. Instead, LEM in either direction occurred with corresponding reduction in sympathetic blood pressure. Diametrically opposite results were found for the non- directional cold pressor stressor. High hostiles were found to be more reactive in their cardiovascular response to stress than the low hostiles.<br>Master of Science<br>[The Beck Depression Inventory, p. 62-66, was removed March 22, 2010 GMc]
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Mollet, Gina Alice. "Hostility and Negative Emotion: Implications for Verbal Learning and Cardiovascular Regulation." Thesis, Virginia Tech, 2004. http://hdl.handle.net/10919/33325.
Full textAbstract:
Hostility is a multidimensional construct that has been extensively studied. It has been shown
that hostility affects cognitive (Shimojima et al., 2003), behavioral (Prkachin & Silverman,
2002), visual (Herridge, Mollet, Harrison, & Shenal, in press), somatosensory (Herridge,
Harrison, & Demaree, 1997a), auditory (Demaree & Harrison, 1997a), motor (Demaree et al.,
2002) and pre-motor functioning (Williamson & Harrison, 2003). In order to extend and
integrate the present literature on hostility and the effects of negative emotional state on
cognition, the present investigation used a cold pressor to induce a negative emotional/pain state
in high and low hostile participants and measured. The subsequent effects on the acquisition of
the Auditory Affective Verbal Learning Test (AAVLT; Snyder & Harrison, 1997) were measured. Blood pressure (BP) readings were taken before and after the cold pressor to examine cardiovascular regulation in high and low hostiles. Further, before the first trial participants were
asked to predict the number of words that they would be able to recall on the first trial. After
completion of the experiment participants were asked to estimate their performance relative to
other participants. The measures were used to assess self-awareness in high and low hostile
participants, which may be impaired in high hostile individuals (Demaree & Harrison, 1997b).
As expected, high hostiles learned negative emotional words significantly better than they
learned positive words. Additionally, high hostiles were impaired in their acquisition of verbal
material relative to low hostile participants. Low hostile participants learned more words faster
and reached asymptote sooner. A significant primacy effect for negative emotional words and an
overall better recall of negative information was found. Analysis on each of the four groups of the experiment indicated that participants in the
cold pressor group performed similar to the high hostile participants. The cold pressor facilitated
negative learning and also slowed verbal learning relative to the no cold pressor group.
It was predicted that high and low hostiles would differ on baseline measures of systolic
blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) and that they would
demonstrate increased cardiovascular reactivity in response to the cold pressor. These hypotheses
were not supported. Self-awareness measures also failed to produce significance.
These results support the proposal that high hostiles differ from low hostiles in a number
of modalities. They demonstrate the persistence of negative emotional material. Future work
should address what kinds of implications these factors have on high hostiles in daily
interactions<br>Master of Science
23
Myredal, Anna. "Cardiovascular regulation and vascular structure in prehypertension and coronary heart disease /." Göteborg : Dept. of Molecular and Clinical Medicine, Sahlgrenska Academy at the University of Gothenburg, 2009. http://hdl.handle.net/2077/20809.
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Wijngaarden, Jan van. "Ace inhibitors and cardiovascular regulation the importance of autocrine and paracrine mechanisms /." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 1992. http://irs.ub.rug.nl/ppn/298212978.
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Everhart, Daniel Erik Jr. "Cerebral Regulation of Cardiovascular Functioning and Fluency among Anxious and Nonanxious Men." Diss., Virginia Tech, 1997. http://hdl.handle.net/10919/30497.
Full textAbstract:
This experiment investigated lateralized hemispheric regulation of the autonomic nervous system (ANS) among high anxious and nonanxious university undergraduate men using a novel laboratory paradigm. Specifically, this three phase paradigm entailed the administration of a verbal fluency (left frontal) and nonverbal fluency (right frontal) task with or without the threat of a painful stimulus (cold pressor) to high anxious and nonanxious participants. Thus, the cerebrums are hypothesized to be engaged in a dual-task experience requiring the regulation of the ANS and concurrent performance on the verbal or the nonverbal fluency measure. Given the literature which supports relative right hemisphere activation among anxious individuals, it was hypothesized that high anxious men would (1) demonstrate greater physiological arousal to the cold pressor, (2) perform relatively worse on nonverbal fluency measures and demonstrate greater difficulty regulating cardiovascular functioning, and (3) demonstrate relatively lower nonverbal fluency scores and increased physiological arousal when presented with the nonverbal fluency task and cold pressor stimulus simultaneously. The results are evaluated using three perspectives: Heller's (1993) hypothesis, Kinsbourne's Functional Cerebral Distance principle, and lateralized regulation of the sympathetic and parasympathetic nervous system. The results only partially supported the right hemisphere activation hypothesis for anxious individuals, as many of the significant results were counter to hypotheses. Specifically, high anxious men demonstrated lower verbal fluency scores and greater heart rate during the combined stimulus of the cold pressor and verbal fluency task. The data are supportive of relative anterior deactivation among high anxious men. The discussion extends the findings to present questions regarding cerebral regulation of the ANS. Future experiments which may add to the current understanding of lateralized regulation of the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) are suggested.<br>Ph. D.
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Pivovarova, Olga [Verfasser]. "Cardiovascular, inflammatory and circadian aspects of metabolic regulation in humans / Olga Pivovarova." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1149050721/34.
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Cellini, Nicola. "The Effects Of Sleep On Autonomic Regulation, Cardiovascular Activity, And Cognitive Processing." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423738.
Full textAbstract:
Sleep is a cyclical behaviour that occurs every day and we spend a significant portion of our life sleeping. While “why do we sleep” remains an unanswered question, we know that sleep is essential for life. Several aspects of our life are dependent on or strictly related to sleep, from molecular and hormonal levels to high-functional behaviours.
The main purpose of the present dissertation is to investigate through five experiments two of the most fundamental aspects of human life, cardiovascular regulation and cognitive function, in relation to different sleep situations such as healthy and pathological sleep (i.e. insomnia) as well as nocturnal and diurnal sleep. Specifically, the current thesis was aimed to shed further light on some debated aspects of the relationship between sleep and cardiovascular activity (Study 1 and 3) and cognitive abilities (Study 3 and 4) in young adults with insomnia. Moreover, the present dissertation aimed to investigate, to our knowledge for the first time, cardiac autonomic activity during daytime sleep (Study 2) and the effect of sleep on selective attention (Study 5).
During sleep, we observed a predominant control of the parasympathetic branch of the ANS and a reduction of sympathetic activity. Thus, during sleep the cardiovascular system “takes a break” and reduces its activity compared to wakefulness, when the sympathetic system is predominant. Interestingly, our results showed a similar cardiac autonomic pattern in diurnal sleep. Thus, it appears that it is sleep itself, rather than a specific moment of the day, that is responsible for this cardiovascular break and that daytime sleep can also act as a cardio-protective period. However, when sleep is disturbed, such as in insomnia, the autonomic balance becomes dysfunctional, with a continuously high sympathetic activity. This elevated cardiovascular activity in insomniacs occurs not only during sleep but also during daytime wakefulness. Indeed, we observed a dysfunctional cardiac autonomic profile during sleep and an elevated cardiovascular activity at rest and during the execution of cognitive tasks in young individuals with disturbed sleep. When this period is disturbed, such as in insomnia, the autonomic regulation becomes dysfunctional, leading to an elevated cardiovascular activity which expose individuals to possible long-term cardiovascular risk.
We also confirm the key role of sleep in cognitive functioning. In healthy individuals we observed a well-established “sleep effect”, i.e. the sleep-related enhancement of procedural memory. However, insomniacs did not show this effect. Also, in insomniacs we observed working memory impairments. Thus, it seems that a disturbed sleep can not only directly impact nighttime cognitive processing (i.e. the sleep-related memory consolidation), but can also affect daytime cognitive functions such as working memory. In addition, we documented the role of sleep in the improvement of attentional abilities, showing a relationship between light sleep and sleep spindles with the magnitude of improvement.<br>Ognuno di noi trascorre una parte significativa della propria vita dormendo. Tuttavia, ad oggi la domanda “perché si dorme?” è ancora senza risposta. Nonostante ciò sappiamo che il sonno è un elemento fondamentale della nostra vita. Lo scopo principale della presente tesi è indagare il rapporto tra sonno e due aspetti vitali della vita umana, la regolazione cardiovascolare e il funzionamento cognitivo. In particolare, nella presente tesi sono stati studiati alcuni aspetti ancora poco chiari del rapporto tra sonno, attività cardiovascolare (Studio 1 e 3) e capacità cognitive (Studio 3 e 4) in giovani adulti con insonnia. Inoltre, nella presente dissertazione è stata investigata l'attività autonoma cardiaca durante il sonno diurno (Studio 2 ) e l' effetto del sonno sull’attenzione selettiva (Studio 5 ).
I nostri risultati mostrano come durante il sonno l’attività autonoma prevalente sia quella parasimpatica, mentre l'attività simpatica tenda a ridursi. I risultati sembrano inoltre indicare come durante il sonno il sistema cardiovascolare "si riposi”, riducendo la sua attività rispetto alla veglia quando è il sistema simpatico a predominare. I nostri risultati hanno anche mostrato come durante il sonno diurno il profilo dell’attività cardiaca autonoma fosse simile a quello notturno. Questi dati indicano come sia il sonno stesso, piuttosto che uno specifico momento della giornata, a facilitare questo “rilassamento” cardiovascolare suggerendo come anche il sonno diurno possa fungere come periodo cardio-protettivo. Tuttavia quando il sonno è disturbato, come nell’insonnia, il bilanciamento autonomo diventa disfunzionale, in quanto caratterizzato da una costante ed elevata attività simpatica. Negli insonni questa elevata attività cardiovascolare sembra essere presente anche durante la veglia diurna. Abbiamo infatti osservato negli insonni sia un profilo autonomo disfunzionale durante il sonno sia un’elevata attività cardiovascolare a riposo e durante l'esecuzione di compiti cognitivi. Quindi quando il sonno è disturbato, come nell’insonnia, la regolazione autonoma diventa disfunzionale portando ad una elevata attività cardiovascolare che espone le persone a possibile rischi cardiovascolari a lungo termine.
Abbiamo inoltre confermato l’importanza del sonno nel funzionamento cognitivo. Abbiamo infatti osservato, in individui sani, come il sonno faciliti il consolidamento e il miglioramento di informazioni procedurali. Tuttavia questo effetto non è stato osservato negli insonni. Inoltre negli insonni abbiamo osservato difficoltà anche a carico della memoria di lavoro. Questi risultati suggeriscono che un sonno disturbato non solo influenzi direttamente l’elaborazione cognitiva durante la notte, come il consolidamento sonno-dipendente delle informazioni, ma influisca anche su altre funzioni cognitive come la memoria di lavoro. Infine, abbiamo descritto il ruolo del sonno nel miglioramento delle capacità attentive, osservando una relazione tra sonno leggero, fusi del sonno e miglioramento attentivo.
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Kakall, Zohra. "Autonomic regulation of medullary neurons following cardiorespiratory, glucoprivic and hypoglycaemic insults." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20798.
Full textAbstract:
The autonomic nervous system (ANS) consists of two divisions: the sympathetic (SNS) and the parasympathetic (PNS) nervous systems. Signal transduction in the ANS requires integration of sensory afferent information from the periphery, central nervous system and spinal cord. Efferent fibres of presynaptic parasympathetic neurons arise from the brainstem and sacral (‘craniosacral’) levels of the spinal cord. There are 5 cranial nerves (CN) that arise from cell bodies located in the Edinger-Westphal nuclei (CN III), superior salivatory nuclei (CN VII), inferior salivatory nuclei (CN IX) and the dorsal motor nuclei of the vagus (CN X), and the nuclei ambiguus of the ventrolateral medulla oblongata (CN X). Sympathetic nerve fibres originate from the remaining thoracolumbar regions in the spinal cord (T1-L3). The sympathetic preganglionic neurons (SPN) residing in the intermediolateral thoracic spinal cord (T5-T12) are relayed via the greater (T5-T9), lesser (T10-T11) and least (T12) splanchnic nerves. The greater splanchnic nerve contains preganglionic fibres that synapse onto the celiac and superior mesenteric ganglion, with the exception of a unique set of long preganglionic sympathetic fibres (forming the adrenal nerve) that synapse onto chromaffin cell bodies in the adrenal medulla. This thesis will focus on diseases and conditions arising from two systems governed by the ANS; namely the cardiorespiratory and endocrine systems. The aim of the introduction is to introduce the essential features (functional anatomy and physiology) of the ANS in terms of the cardiorespiratory and neuroendocrine systems. Secondly, a pathological condition with unknown mechanisms associated with dysfunction of the ANS in each of the cardiorespiratory and neuroendocrine systems will be introduced as separate sub-chapters. Finally, the specific aims and results of the relevant studies will be provided, with emphasis placed on SNS and neuropeptidergic control in each condition.
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Welser, Jennifer Verena. "Regulation of smooth muscle cell phenotype by the a7ß1 integrin." abstract and full text PDF (UNR users only), 2008. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3312248.
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Sund, M. (Malin). "Type XIII collagen: regulation of cardiovascular development and malignant transformation in transgenic mice." Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514265572.
Full textAbstract:
Abstract
Type XIII collagen is a type II oriented transmembrane protein with a short
intracellular domain, a single transmembrane domain and a large, mostly
collagenous extracellular domain. Tissue localization and cell culture studies
have implicated that it is involved in cell adhesion.
The spatio-temporal expression of type XIII collagen mRNA and protein
during murine development is studied here. Type XIII collagen mRNAs were
expressed at a constant rate during development, with an increase of expression
towards birth. The strongest expression was detected in the central and
peripheral nervous systems of the developing mouse fetus. Cultured primary
neurons expressed this collagen, and recombinant type XIII collagen was found to
enhance neurite outgrowth. Strong expression was also detected in the heart, with
localization to cell-cell contacts and perinatal accentuation in the intercalated
discs. Other sites of type XIII collagen expression included cartilage, bone,
skeletal muscle, lung, intestine and skin. Clear developmental shifts in
expression suggest a role in endochondral ossification of bone and the branching
morphogenesis in the lung.
To elucidate the function of type XIII collagen transgenic mice were
generated by microinjection of a cDNA construct that directs the synthesis of
truncated α1(XIII) chains with an in-frame deletion of the central
collagenous
COL2 domain. This construct was thought to disrupt the assembly of normal type
XIII collagen trimers. Expression of shortened α1(XIII) chains by
fibroblasts
derived from mutant mice was demonstrated, and the lack of intracellular
accumulation in immunohistochemical analysis of tissues suggested that the mutant
molecules were expressed on the cell surface. Transgene expression led to
developmental arrest and fetal mortality in offspring from heterozygous mating
with two distinct phenotypes. The early phenotype fetuses were aborted by day
10.5 of development due to a failure in the fusion of the chorion and allantois
membranes and subsequent disruption in placentation, while the late phenotype
fetuses were aborted by day 13.5 of development due to cardiovascular and
placental defects. Furthermore, it was shown that the heterozygous mice that were
initially of normal appearance and bred normally had an increased susceptibility
to develop T-cell lymphomas and angiosarcomas later in life.
The results presented here increase the evidence that type XIII collagen is
involved in cell adhesion, with several important tasks during development. A
role of type XIII collagen in malignant transformation of certain mesenchymal
cell populations is also implicated.
31
Liu, Hanguan. "Expression and regulation of phosphodiesterase 3 and phosphodiesterase 4 in rat cardiovascular tissues." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0007/NQ42955.pdf.
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Creasy, Kate Townsend. "ZHX2 REGULATION OF LIPID METABOLISM AND THE BALANCE BETWEEN CARDIOVASCULAR AND HEPATIC HEALTH." UKnowledge, 2015. http://uknowledge.uky.edu/pharmacol_etds/10.
Full textAbstract:
The growing obesity epidemic in America carries with it numerous health risks, including diabetes, increased serum lipid levels, and excess fat accumulation in the liver. If these conditions persist or become exacerbated, they may lead to the development of cardiovascular disease, the current leading cause of death among Americans, or to nonalcoholic fatty liver disease (NAFLD) which can progress to hepatocellular carcinoma (HCC), one of the deadliest forms of cancer. Better understanding of the genes involved in these diseases can lead to improved identification of at-risk individuals and treatment strategies.
Our lab previously identified zinc fingers and homeoboxes 2 (Zhx2) as a regulator of hepatic gene expression. The BALB/cJ mouse strain has a hypomorphic mutation in the Zhx2 gene, causing a 95% reduction in Zhx2 protein expression. The near ablation of Zhx2 in BALB/cJ mice confers protection from cardiovascular disease when fed a high fat diet, yet these mice show increased hepatic lipid accumulation and liver damage. Microarray data indicates Zhx2 may be involved in the regulation of numerous genes involved in lipid metabolism. Recent GWAS studies indicate ZHX2 may contribute to the risk of cardiovascular disease and liver damage in humans as well.
In this dissertation, I characterize the role of Zhx2 expression in the liver and how it affects the risk of both cardiovascular disease and liver damage. I generated liver-specific Zhx2 knockout mice and confirmed Zhx2 regulates several novel targets that could contribute to the fatty liver phenotype seen in BALB/cJ mice. Further studies revealed that hepatic Zhx2 expression is necessary for proper sex-specific expression of several Cyptochrome P450 (CYP) genes and could contribute to gender differences in disease susceptibility. Lastly, I performed studies into the functional role of the Zhx2 target gene Elovl3. A mouse model of HCC revealed that Elovl3 is completely repressed in HCC tumors. Cell viability and cell cycle assays indicate that Elovl3 expression slows cell proliferation and may be important for proper cell cycle checkpoints. Together, these data indicate that Zhx2 and/or its targets could be clinically relevant in the detection, prevention, or treatment of cardiovascular disease, fatty liver, and HCC.
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Sun, Bing, and 孫冰. "Vestibular influence on central cardiovascular regulation in the rat: functional and anatomical aspects." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31244774.
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Raine, Neil Martin. "Cardiovascular adjustments and blood pressure regulation immediately following dynamic exercise in normotensive men." Thesis, Liverpool John Moores University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388524.
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Beda, Alessandro. "Cardiovascular and respiratory responses to psychophysiological tasks : methodological issues for assessing autonomic regulation." Thesis, University of Southampton, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440413.
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Rook, William. "The effects of chronic hypoxia in utero on cardiovascular regulation in the offspring." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/3040/.
Full textAbstract:
A common consequence of the complications of pregnancy, such as preeclampsia, is reduced supply of nutrients, including oxygen, to the developing fetus. The consequences for the offspring are wide ranging, but include increased risk of cardiovascular disease. However, the mechanisms by which this occurs are poorly understood. Using a rodent model, this study has examined the regulation of blood vessels, particularly those supplying skeletal muscle, by local, endothelially-derived factors, and by the sympathetic nervous system, in adult rat offspring following chronic hypoxia in utero. The key findings include evidence that there are chronically high levels of oxidative stress in the skeletal muscle vasculature of the offspring. Further, the density of, and the activity in the sympathetic neurones supplying skeletal muscle blood vessels is markedly increased following chronic hypoxia in utero, but the vascular sensitivity to stimulation of these neurones is reduced. Following chronic hypoxia in utero, as the rats approached middle age, they became hypertensive relative to normal rats. Thus, the present study has offered some mechanistic insight, which adds to a growing body of literature, and which may help to explain why babies born of sub-optimal pregnancies are at higher risk of developing cardiovascular disease later in life.
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Bodkin, Jennifer. "Investigating the role of Transient Receptor Potential Ankyrin One (TRPA1) in cardiovascular regulation." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-the-role-of-transient-receptor-potential-ankyrin-one-trpa1-in-cardiovascular-regulation(86e661c9-d299-45cd-b3d3-b23fe18f9181).html.
Full textAbstract:
TRPA1 is a member of the TRP superfamily; localised to neural and non-neuronal sites. TRPA1 is activated endogenously by products of oxidative stress, where its expression on sensory neurones leads to the release of vasoactive neuropeptides. Exogenous agonists of TRPAl, mustard oil and cinnamaldehyde, have been shown to cause concentration-dependent vasorelaxation of blood vessels via a variety of mechanisms. My PhD used TRPA1 WT and KO mice to investigate the potential for TRPA1 to alter peripheral artery tone and the implications of this on systemic blood pressure. I also studied the development of angiotensin II induced hypertension and associated pathologies. Wire myography using murine TRPA1 WT and KO mesenteric arteries showed cinnamaldehyde to cause concentration-dependent vasorelaxation comprising a TRPA1 dependent component, which was endothelial independent and mediated by CGRP and hyperpolarisaton. Basal blood pressure monitoring by both tail cuff plethysmography and telemetry showed no overall effect of TRPA1 deletion on basal hemodynamics. However, TRPAl KO mice displayed a previously unreported hyperactivity phenotype, measured by both telemetry and voluntary wheel running. 14 day infusion of angiotensin II by osmotic minipump induced similar hypertension in both TRPA1 WT and KO mice. Hypertrophy of the heart was seen in both genotypes, but of significantly increased magnitude in TRPA1 KO mice. Further analysis of associated inflammatory biomarkers by RT qPCR and MSD multiplex ELISA showed upregulation of pro-oxidative genes in hypertensive mice of both genotype. This was significantly greater in hypertensive TRPA1 KO mice than in hypertensive TRPA1 WT mice. These findings may partially explain the increase in hypertrophy in these mice. Angiotensin II infused mice of both genotypes showed increases in chemokine and cytokine expression. Striking, increases in IL6 and MCP-1 seen in hypertensive WT mice were significantly blunted in hypertensive KO mice, suggesting that TRPAl may differentially modulate inflammatory responses.
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Shenal, Brian V. "Dynamic Effects of Stress and Hostility: Group Differences in Cardiovascular Regulation and Learning." Diss., Virginia Tech, 2000. http://hdl.handle.net/10919/27464.
Full textAbstract:
This experiment tested hypotheses linking the right cerebral regulation of hostility and cardiovascular reactivity. First, replication of previous research supporting heightened cardiovascular reactivity (mean arterial pressure, systolic blood pressure, diastolic blood pressure, and heart rate) among high-hostile participants was attempted. Second, dynamic variations in functional cerebral asymmetry in response to pain (cold pressor stressor) and affective verbal learning (positive and negative valenced word lists) were measured.
High- and low-hostile participants (n = 64) were identified using the Cook Medley Hostility Scale. Participants completed either the cold-pressor stressor condition or the no-stress control condition as well as the negative and the positive affective verbal learning test. Cardiovascular measures (MAP, SBP, DBP, and HR) before and after the stress or no-stress condition and before and after the negative and the positive affective learning tasks were recorded.
The results demonstrated that high-hostiles had difficulty processing emotional stimuli. High-hostiles were reliably impaired in emotional word learning. Further, results suggested that negative affective learning produced proactive interference for the learning or recall of subsequently presented information. Positive affective learning produced diametrically opposite effects with retroactive interference for the recall of previously presented information. Also, high-hostiles' cardiovascular reactivity to a physical stressor was independent of the valence of the learning task. In contrast, low-hostiles' cardiovascular reactivity was valence dependent with activation to both the positive list concurrent with stress and to the negative list concurrent with no stress. Finally, the results indicated that the effect of the affective learning lists, on the heart, is stress dependent. Neuropsychological theories of ANS regulation and emotion are discussed in relation to the primary findings and a new model of lateralized regulation is proposed.<br>Ph. D.
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Cummins, James B. "Adrenergic and Cholinergic Regulation of Cardiovascular Function in Embryonic Neotropic Cormorants (Phalacrocorax basilianus)." Thesis, University of North Texas, 2017. https://digital.library.unt.edu/ark:/67531/metadc984219/.
Full textAbstract:
Investigations of cholinergic and adrenergic tone on heart rate (fH) and mean arterial pressure (Pm) during embryonic development have been conducted on numerous avian species. While these investigations have documented that adrenergic tone, a continuous stimulation, on fH and Pm is vital to embryonic development in the birds studied to date, development of cholinergic tone on fH has been shown to vary even within species. Further, past studies have been bias to focus primarily on precocial species while altricial species remain poorly understood in this context. The goal of this investigation was to investigate the role of cholinergic and adrenergic tone on fH and Pm of an altricial species, the neotropic cormorant (P. brasilianus) to address this bias. The embryonic neotropic cormorant possesses B-and-a adrenergic tone on fH and Pm at 70% and 90% incubation while cholinergic tone on fH occurs at 90% incubation. This pattern of control is similar to that previously reported for several species of precocial birds suggesting the development of tonic cardiovascular regulation may be conserved across avian taxa.
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Littlejohn, Nicole Kathryn. "Tissue-specific roles for the renin-angiotensin system in cardiovascular and metabolic regulation." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/2236.
Full textAbstract:
The renin-angiotensin system (RAS) greatly contributes to energy homeostasis through opposing actions in the brain and adipose. We hypothesize that site- and receptor-specific effects of the RAS may represent a novel therapeutic target for obesity, a concept which is fully reviewed in chapter 1. Transgenic “sRA” mice exhibit brain-specific RAS hyperactivity, and a suppressed circulating RAS presumably secondary to the chronic hypertension exhibited by these animals. In chapter 2, we demonstrated that the hypertension observed with elevated brain RAS is mediated by increased vasopressin signaling. In chapter 3, we investigated how suppressed circulating RAS activity contributes to the elevated resting metabolic rate (RMR) of sRA mice. Despite having no effect upon energy intake, chronic angiotensin II type 2 (AT2) receptor activation suppressed energy expenditure and caused weight gain in sRA mice. The AT2 receptor alters inguinal white adipose tissue to contribute to obesity through the suppression of RMR. Lastly, in chapter 4, we documented moderately-improved glycemic control with elevated brain RAS/reduced circulating RAS activity, though the mechanism behind this remains unknown. Taken together, we determined that low circulating RAS activity is metabolically beneficial due to reduced activation of the AT2 receptor. Thus, specific inhibition of the systemic RAS may ultimately stimulate energy expenditure and thus may be a viable anti-obesity pharmaceutical approach. Overall, our data highlight the importance of site-specific effects of the RAS on energy homeostasis.
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SATHER, TOM MALVIN. "MECHANISMS OF CARDIOVASCULAR ADJUSTMENTS ASSOCIATED WITH PRESYNCOPAL-LIMITED LOWER BODY NEGATIVE PRESSURE TOLERANCE (ORTHOSTASIS)." Diss., The University of Arizona, 1985. http://hdl.handle.net/10150/188096.
Full textAbstract:
In man, tolerance to an orthostatic stress varies widely. Compensatory cardiovascular responses to orthostatic stressors such as head-up tilt, +Gz acceleration, and lower body negative pressure (LBNP) have been identified. However, physiologic reactions associated with the capacity to withstand a presyncopal- limited orthostatic exposure requires additional clarification. The relationship between maximal oxygen uptake (‘VO₂ max) and presyncopal-limited LBNP tolerance was examined in adult male subjects categorized into high (HAC) and low (LAC) aerobic capacity groups. In addition to similar (N.S.) cardiovascular responses, the (mean) and cumulative LBNP stress indices (CS)) observed in the HAC (722 torr•min) and LAC (784 torr•min) groups were also similar (N.S.). These data fail to support a relationship between LBNP tolerance and ‘VO₂ max. Cardiovascular responses associated with LBNP tolerance were measured during the control period (pre-LBNP) and final minute (peak LBNP) of decompression. The CSI criterion distinguished high (HT, n = 10) and low (LT, n = 8) LBNP tolerant groups was 640 torr•min. A greater (p < 0.05) end-diastolic volume and cardiac output was observed in the HT subjects during pre-LBNP may have provided a larger reserve to utilize throughout exposure to LBNP. At peak LBNP, both groups demonstrated similar (N.S.) cardiac outputs despite a higher (p < 0.05) HT heart rate. These data suggest that a major mechanism in prolonging LBNP tolerance may have been a greater LBNP-induced tachycardia. Blood samples were drawn to determine group differences in vasoactive neuroendocrine response. During peak LBNP, concentrations of norepinephrine increased (p < 0.05) in both groups. The HT group displayed greater (p < 0.05) LBNP-induced increases in vasopressin and plasma renin activity. These data suggest that HT subjects may have supplemented the catecholamine pressor response by involving the vasopressin and renin-angiotensin systems. The affect of cholenergic and beta-adrenergic blockades on cardiovascular responses to LBNP were examined in six HT and five LT subjects. CSI in both groups were unchanged (N.S.) by administration of atropine as compared to a placebo LBNP exposure. Propranolol however, reduced (p < 0.05) LBNP tolerance in both groups. This CSI reduction was greater (p < 0.05) in the HT subjects. The reduction in LBNP tolerance appeared closely associated with the negative chronotropic effect.
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Pikkujämsä, S. (Sirkku). "Heart rate variability and baroreflex sensitivity in subjects without heart disease:effects of age, sex and cardiovascular risk factors." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514252276.
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Abstract
Healthy subjects show wide interindividual variation in their
heart rate behavior, but the factors affecting heart rate dynamics
are not well known. This research was undertaken to evaluate heart
rate variability (HRV) and baroreflex sensitivity (BRS) in a large
random sample of subjects without evidence of heart disease, and
to estimate the relation of heart rate behavior to age, sex and
cardiovascular risk factors.
Short-term HRV was analyzed from 15-minute periods of standardized
recording in supine and upright positions using time and frequency
domain measures, and BRS was calculated using the Valsalva maneuver
in an original randomly selected population of 600 hypertensive
and 600 control middle-aged subjects. In addition, HRV was analyzed
from the same segments using new measures based on fractals and
complexity (chaos theory) of R - R interval dynamics in
the same random population, and from 24-hour period in 114 healthy
subjects aged from 1 to 82 years.
Large interindividual variation was observed in the measures
of HRV and BRS in middle-aged subjects; coefficient of variation
(CV) of the standard deviation of R - R intervals (SDNN)
39% (54 ± 21 ms) and CV of BRS 49% (9.9 ± 4.9
ms/mmHg). In healthy middle-aged men, SDNN was weakly related
to age (r = -0.19, p < 0.01),
HDL cholesterol (0.19, p < 0.01), serum
insulin (-0.23, p < 0.001) and triglyceride
(-0.25, p < 0.001) levels.
In women, SDNN was only related to insulin levels (r = -0.23,
p < 0.001). BRS was related to systolic
blood pressure (r = -0.31 and -0.30,
in men and women respectively, p < 0.001
for both) and blood glucose (r = -0.25,
p < 0.01) and serum insulin levels (r = -0.34,
p < 0.001) in women. Lesser intersubject
variation was observed in the non-linear measures of HRV; CV 14% of
short-term scaling exponent (a1), a measure of fractal-like correlation
properties of HRV, (1.21 ± 0.17) and
CV 12% of approximate entropy, a measure of complexity,
(1.13 ± 0.14). Neither a1 or ApEn was
related to any risk factors. Women had lower overall short-term
HRV (p < 0.01) and BRS (p < 0.001),
but a higher spectral high-frequency component of HRV, higher ApEn
and lower a1 (p < 0.001 for all) compared
to men. The impairment in overall HRV was confined to the hypertensive
subjects with metabolic features of the insulin resistance syndrome
(IRS, n = 69), but the BRS and spectral
high-frequency component were also impaired in hypertensive subjects
without IRS compared to normotensive subjects. The 24-hour cardiac
interbeat interval dynamics changed markedly from childhood to
old age. Children showed similar complexity and fractal correlation
properties of R - R intervals as young adults. Healthy aging
resulted in R - R interval dynamics with higher regularity
and predictability and altered fractal scaling.
The traditional measures of HRV and BRS are weakly related
to many cardiovascular risk factors in subjects without heart disease,
but the interindividual variation of HRV and BRS is only partly
explained by these factors, suggesting a genetic background of
the intersubject variation in cardiovascular autonomic regulation.
The new dynamical measures of HRV show less interindividual variation
than the conventional measures of HRV in healthy subjects and are
not related to cardiovascular risk variables, suggesting that these
dynamical measures quantify the "intrinsic" capacity of a healthy
cardiovascular control system without the significant influence
of life-style, metabolic or demographic variables. However, there
are sex and age-related differences also in the fractal and complexity
measures of heart rate behavior.
43
Wood, David Rowe Ding Jiahuan. "Design, optimization, and evaluation of conditionally active gene therapy vectors." Waco, Tex. : Baylor University, 2008. http://hdl.handle.net/2104/5153.
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Le, Cras Timothy David. "Regulation of the levels of mRNA for the LDL receptor and HMG CoA reductase." Thesis, University of Cambridge, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239497.
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Royal, Alice. "The regulation of trafficking and function of KCNQ1 potassium channels by phosphatidylinositol-4,5-bisphosphate." Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/25940.
Full textAbstract:
The IKs current constitutes part of the repolarisation reserve in the human myocardium, and whilst it does not play a major role at resting heart rates, it becomes a crucial component of repolarisation in the setting of increased sympathetic tone and high heart rates. The formation of the IKs current requires the KCNQ1 α-subunit and the KCNE1 β-subunit. Mutations in either of these subunits can lead to long QT syndrome types 1 and 5, respectively. Loss-of-function mutations in the IKs channel can reduce the repolarisation reserve and lead to action potential prolongation, predisposing to lethal cardiac arrhythmias such as torsades de pointes and ventricular fibrillation. It is widely recognised that the IKs channel requires the minor membrane phospholipid PIP2 for its function, and previous work in this laboratory found that mutations in a PIP2-binding region in KCNQ1 led to retention of the channel in the endoplasmic reticulum, suggesting that PIP2 may play a role in anterograde trafficking. Here, the rapamycin-inducible dimerisation system was used to manipulate levels of PIP2 and/or PI4P at the plasma membrane or Golgi, and the effect of this on IKs channel trafficking and function was investigated using molecular biology, confocal microscopy and electrophysiology. Despite difficulties with optimising the rapamycin-induced dimerisation system, it was observed that the IKs channel does not require PIP2 for anterograde trafficking, but is heavily reliant on PIP2 for channel opening. In addition, activation of the β1-adrenergic receptor (β 1-AR) led to an increase in the IKs current amplitude. The potential interplay between β1-AR and PIP2 signalling was also explored by depleting PIP2 during β1-AR stimulation. PIP2 depletion was less effective at inhibiting the IKs current during β1-AR stimulation, but this requires further investigation. In conclusion, the results suggest that the IKs channel is reliant on PIP2 for function, but not anterograde trafficking.
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Higgins, Dane Allen. "A Neuropsychological Investigation of Sex Differences in Cardiovascular Reactivity to Verbal and Spatial Fluency Tasks: Testing a New Model of Sex Differences in Cardiovascular Regulation and Disease." Diss., Virginia Tech, 2002. http://hdl.handle.net/10919/27628.
Full textAbstract:
One hundred twenty-six right-handed undergraduate men and women underwent physiological measurements of SBP, DBP, and HR before and after verbal and figural fluency tasks, used as stressors. Dynamic and functional cerebral regulation of cardiovascular reactivity was assessed, specifically, the role that the frontal lobes have in regulating SBP, DBP, and HR in men and women. Sex differences in the functional cerebral regulation of these cardiovascular factors were predicted. Hostility was assessed in these participants, using the Cook-Medley Hostility Inventory (6 total groups of 21 participants each: high-, mid-, and low-hostile participants were identified). Sex and group (hostility) differences were predicted, as well as task (fluency type) differences. Comparisons were also made from a time estimation task (30 and 180 seconds), and the effect that womenâ s menstrual cycle had on fluency. The MCSDS and the STAI were administered.
The principal findings of the current investigation were that the verbal fluency task raised SBP across sex and group, that both stressors raised SBP or DBP in different patterns (no sex differences were found), while stressors interacted with both sex and group. High-hostile men performed better on the first trial of the verbal fluency test compared to low-hostile men, while high-hostile women performed worse on the first trial of the verbal fluency test, compared to low-hostile women. Men perseverated more on each trial of the verbal fluency test, while women perseverated less across trials. High-hostile menâ s time perception seems to be more rapid than low-hostile men, while for women it is the opposite. Women reported significantly more stress from the figural fluency task than men. Women in the luteal phase of menstruation did better on the verbal fluency test than women in the follicular phase of menstruation, and hostility and menstrual phase interact with verbal fluency.
This study encourages the consideration of neuropsychological sex differences in order to better understand cardiovascular regulation mechanisms and disease, leading to the development of improved prevention and behavioral management programs. Findings supporting this idea may bring about a new research focus, as some forms of cardiovascular disease may be more appropriately investigated as arising from neuropsychological problems.<br>Ph. D.
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Hunter, Kirsty A. "Studies of the regulation of plasma protein synthesis in man using stable isotopes." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU543871.
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Metabolism of the transport protein albumin is known to be regulated by long-term nutrient status. To assess the short-term response to feeding, studies were performed which measured the rate of albumin synthesis once after an overnight fast and once after one of two feeding regimens consisting of five small hourly meals or one large meal. Albumin synthesis increased by approximately 25% and 31% above the fasting value for the small meals and large meal regimens respectively, thus demonstrating that albumin synthesis is acutely sensitive to nutrient intake. A supplementary animal experiment indicated that this response is part of an overall increase in liver protein synthesis. Elevated plasma fibrinogen concentration has been implicated as a risk factor for the development of cardiovascular disease. As cigarette smokers are known to have a significantly raised plasma fibrinogen concentration, studies were performed to investigate the metabolic mechanism responsible for this by comparing the rate of fibrinogen synthesis in smokers and non-smokers and smokers who had abstained from smoking for 14 days. Smokers had a significantly greater absolute rate of fibrinogen synthesis (mean SD, 21.5 1.9 versus 16.0 1.4 mg/kg/d, p<0.05). Although smokers were found to have moderate leucocytosis, there did not appear to be any increased metabolic activity of lymphocytes. In a separate group of smokers, abstention from smoking for 14 days resulted in a significant reduction in plasma fibrinogen concentration of 19%. The fractional rate of fibrinogen synthesis also decreased significantly by 14% suggesting that a substantial part of the hyperfibrinogenaemia observed in smokers is the product of increased output by the liver.
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Rhodes, Robert D. "Frontal Lobe Correlates in Hostile Men: Analysis of Facial Motor Tone and Cardiovascular Regulation." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/37723.
Full textAbstract:
This experimented proposed to test the relationships between self-reported hostility and both facial muscle tone and cardiovascular functioning. Based on previous research, it was proposed that individuals high in self-reported hostility would show increased cardiovascular reactivity in response to a physical stressor (the cold-pressor task). Additionally, based on the integration of multiple lines of research, it was proposed that individuals with high levels of self-reported hostility would show asymmetric facial tone, with greater muscle activation at the left-hemiface. Results showed increased cardiovascular responding in the high-hostile participants following exposure to the cold-pressor task. Additionally, the individuals with high levels of self-reported hostility did show asymmetric facial tone, with increased left-hemifacial EMG values. These differences were present prior to exposure to the cold-pressor task, and were increased following the stressor. Results supported the literature showing increased cardiovascular responding to stress in high-hostile individuals, and also supported the proposed relationship between right orbitofrontal functioning and hostility.<br>Ph. D.
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Cruickshank, Nicholas Christopher. "The Effects Of Hypothalamic Brain-Derived Neurotrophic Factor On Catecholaminergic Regulation Of Cardiovascular Function." ScholarWorks @ UVM, 2017. http://scholarworks.uvm.edu/graddis/804.
Full textAbstract:
Considerable evidence supports the claim that a hyperactive sympathetic nervous system (SNS) is involved in most cases of human hypertension, and therefore a more thorough understanding of the central regulation of the SNS may help elucidate novel therapeutic options. The PVN is a key region in SNS regulation of blood pressure (BP) and heart rate (HR). Stimulation of the parvocellular PVN neurons has been shown to enhance sympathetic outflow and thereby increase BP. Brain-derived neurotrophic factor (BDNF), a modulator of neuronal activity is upregulated in the paraventricular nucleus of the hypothalamus (PVN) in response to several hypertensive stimuli such as stress and hyperosmolarity, and previous studies from our lab demonstrated that both acute injections or chronic overexpression of BDNF in the PVN elevate SNS activity and BP. However, the BDNF-mediated hypertensive mechanisms are not completely understood. PVN neurons are under tonic inhibition from NTS catecholaminergic projections under baseline condition as indicated by significant BP increase after selective lesioning of NTS NE-ergic neurons. In addition, BDNF has been shown to alter NE-ergic signaling in multiple brain regions raising the possibility that BDNF may increase SNS activity and BP by interfering with NE-ergic inhibition of PVN sympathoregulatory neurons. Therefore, we tested the hypothesis that BDNF increases SNS activity and BP in part by disabling inhibitory actions of NTS catecholaminergic projections to the PVN by altering the expression of adrenergic receptors and NET in the PVN.
First, blood pressure was recorded using radiotelemetry in male Sprague-Dawley rats following bilateral microinjections of adeno-associated viral vectors expressing green fluorescent protein (GFP) or myc-tagged BDNF in the PVN and microinjections of phosphate saline buffer (PBS) or Anti-Dopaine Beta Hydroxylase (DBH)-conjugated saporin (DSAP), a catecholaminergic neuron-specific neurotoxin, into the NTS. Blood pressure was monitored both during resting conditions and during acute stress tests. A second group of rats received bilateral microinjections of adeno-associated viral vectors expressing GFP or myc-tagged BDNF in the PVN, and were sacrificed after 5 weeks. PVN and NTS samples were then selectively isolated using a brain punch tool, and expression of TH, DBH, 1a, 1b, 2a, 1, 2 receptors, and norepinephrine transporter (NET) was analyzed using quantitative RT-PCR.
Our results show that BDNF overexpression in the PVN leads to increased expression of catecholamine synthesizing enzymes in the NTS. In addition, both BDNF overexpression in the PVN, and DSAP lesioning in the NTS increased MAP compared to control rats. However, combined treatment with BDNF and DSAP failed to have any additional hypertensive effects suggesting that BDNF treatment may abolish the inhibitory effect of NTS catecholaminergic projections. Lesioning the NTS catecholaminergic neurons didn’t appear to have a significant effect on mean arterial pressure response to the stress tests, although DSAP treatment appeared to decrease the initial heart rate response to acute stress, and this effect was most pronounced in GFP rats. These results indicate that BDNF overexpression in the PVN desensitizes sympathoregulatory neurons to inhibitory NTS catecholaminergic projections during baseline conditions.
50
Gunner, David J. L. "Role of gut hormones in the regulation of appetite and modulation of cardiovascular function." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501466.
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