Dissertations / Theses: 'Blood pressure regulation'

1

Johnson, J. V. "Vasopressin and blood pressure regulation in the rat." Thesis, University of Nottingham, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376525.

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2

Galla, Sarah L. "Studies on the Holobiont and Blood Pressure Regulation." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1556099980339015.

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3

Peirce, Susan Caroline. "Investigating short-term blood pressure regulation : peripheral baroreceptor sensitivity." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29891.

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Autonomically-mediated baroreflex control of heart rate has been extensively studied (cardiac BRS, cBRS), but peripheral control of blood pressure is less well known. Total peripheral resistance (TPR) was derived from pulse contour stroke volume (SVPC) using non-invasive blood pressure (Finapres). The beat-to-beat variability of Finapres SVPC was evaluated in cardiac catheterisation patients against aortic blood pressure SVPC. Correlations were generally good (mean R = 0.75), but regression slopes tended to be less than unity and several aortic recordings were significantly affected by the dynamic response of the measurement system. Finapres SVPC was also compared to Doppler stroke distance (SD) in healthy volunteers. Both measures followed respiratory movements well, although SVPC had higher coherence with respiration. Discrepancies between the results were considered to be mainly due to errors in the Doppler method. Coherence thresholds for spectral cBRS were determined as a function of the number of subrecords available for ensemble averaging and the effect of ventricular ectopics on cBRS estimates was investigated. Pulse contour TPR data was then used to determine peripheral BRS (pBRS) in healthy controls and neurocardiogenic syncope patients (NCS) using methods adapted from cardiac BRS analysis. Diastolic pressure produced greater pBRS estimates than systolic pressure and pBRS was generally higher in patients and fainters than in controls and non-fainters. Tilt did not have a consistent effect on pBRS and it was not linearly related to age or resting blood pressure, although it may be increased in hypertension and the elderly. pBRS was able to discriminate between the subject groups when cBRS methods showed no difference.

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4

Ashraf, Usman Mohammad. "Novel Regulators of Kidney Homeostasis and Blood Pressure Regulation." University of Toledo Health Science Campus / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=mco1596206028212986.

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5

Correia, Anabela G. 1975. "The renal medullary circulation and blood pressure control." Monash University, Dept. of Physiology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8480.

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6

Lopez, Kyle Eric, and Kyle Eric Lopez. "Uncovering Signal Transduction in Blood Pressure Regulation by Nitric Oxide." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625045.

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Nitric Oxide (NO) is an important signaling molecule in blood pressure regulation. The NO receptor, soluble guanylate cyclase (sGC), produces the secondary messenger cGMP in response to NO binding. Because of its role in blood pressure regulation, sGC is increasingly targeted for drug discovery and several new drugs treating hypertensive individuals are sGC stimulators. Unfortunately, stimulator development is limited by our understanding of NO and simulator induced conformational changes. In the present study, we used lanthanide resonance energy transfer (LRET) to measure distances between sGC domains in truncated M. sexta sGC constructs and assessed the magnitude of distance changes induced by ligand binding. Our strategy was to place a lanthanide binding domain at various locations in the protein and measure changes in lanthanide luminescence in the presence of the quenching domain, His6 with coordinated copper or nickel ion, which quenches luminescence in a distance dependent manner. Terbium luminescence decayed bi-exponentially in the absence of quencher, and displayed a slow phase with a rate constant of ~2.3 ms. Quencher presence altered the time constant for the slow phase, but not the fast phase. Distances obtained from fitting these data indicate sGC is a compact molecule with the coiled-coil ~23 Å from the a H-NOX N-terminal end. However, we must further develop our system to ensure the decays measured reflect the distance between donor and acceptor. In the future, distances will be measured after ligand or stimulators are bound to determine the change in distance, which will give insight into the conformational dynamics of sGC.

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7

Huang, Chunhua. "Impact of dietary salt intake during growth on cardiovascular homeostasis and neural control of the kidney : role of brain angiotensin II (Ang II)." Thesis, University of Birmingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368519.

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8

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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9

Muzs, Karolin. "The influence of short chain fatty acids on blood pressure regulation." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=236055.

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Hypertension is a widespread condition which may cause cardiovascular events when left untreated. If high blood pressure (BP) is noticed at all, it is mostly only sub-optimally controlled making nutritional interventions a cost-effective and safe preventive measure and an alternative to medical treatment. Previous studies have shown that increased fibre consumption reduces BP which was particularly effective in hypertensive subjects. Fibres are indigestible and hence are available for fermentation by the colonic microbiota which produces the short chain fatty acids (SCFAs) acetate, propionate and butyrate. Intriguingly, recent studies carried out in mice showed that SCFAs can reduce BP. Therefore, we hypothesised that gut microbiota-derived SCFAs can (1) reduce BP in middle-aged male volunteers and (2) influence the protein expression of BP regulatory systems in a cellular model. As the development of a cellular angiotensin II-induced hypertension model was unsuccessful, the effects of SCFAs on a molecular level were assessed in unstimulated human aortic endothelial cells (HAECs). The expression of proteins involved in the BP regulating renin angiotensin system (RAS) was assessed by western blotting. Additionally, a human supplementation trial is being carried out looking at the acute consumption of a low (0.16 g) and high (2.35 g) propionate dose on BP and other cardiovascular markers in middle-aged male volunteers. In vitro work showed that SCFAs did not affect RAS expression in HAECs. However, acute propionate supplementation influenced BP and its regulation. Preliminary data show, that while a high propionate dose led to increases in plasma propionate by on average 4 µM and acetate levels with concurrent increases in BP, arterial stiffness and plasma renin concentration, a low propionate dose resulted in plasma propionate increases of about 0.5 µM with simultaneous reductions in systolic BP. Taken together, these results suggest that SCFAs play a regulatory role in the homoeostasis of BP.

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10

Rahsid, Imad Hatim. "Role of C1-adrenergic neurones in the regulation of vasopressin and pressor response." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294526.

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11

Hammad, Sally. "The role of PMCA1 in blood pressure regulation and the development of hypertension." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-pmca1-in-blood-pressure-regulation-and-the-development-of-hypertension(61b800d1-26a5-44ae-8d50-5e72676c555e).html.

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Introduction: Hypertension is a complex disease that affects about 40% of adults worldwide, and is a major risk factor for cardiac hypertrophy and heart failure. Abnormal calcium handling plays a key role in hypertension and cardiovascular disease. In order to function normally cells of the cardiovascular system need to keep intracellular Ca2+ levels under tight control. This is achieved by a number of Ca2+ handling proteins including the plasma membrane Ca2+-ATPase (PMCA). Recent genome wide association studies have shown that single nucleotide polymorphisms in ATP2B1, the gene encoding PMCA1, are strongly linked with hypertension risk. Hypothesis: PMCA1 plays an important role in regulation of blood pressure and protection against hypertension and cardiac hypertrophy. Aims: This thesis aims to examine whether there is a link between PMCA1 and blood pressure regulation, and the development of hypertension. It also aims to determine the impact this link may have on cardiac structure and function. Methods and Results: To study the role of PMCA1, a global PMCA1 heterozygous knockout mouse (PMCA1Ht) was used. Under basal conditions, 3 month old PMCA1Ht mice had about 50% reduction in PMCA1 protein expression compared to the wild type (WT) mice. PMCA1Ht and WT mice had similar blood pressure as measured by tail-cuff method. To study the mice under hypertensive stress conditions, 3 month old PMCA1Ht and WT mice were infused via minipump with angiotensin II. Upon angiotensin II treatment, PMCA1Ht mice showed a significantly greater increase in systolic and diastolic pressure compared to WT mice. Angiotensin II also induced vascular remodelling, with PMCA1Ht mice having greater media thickness and cross sectional area than WT mice. Moreover, PMCA1Ht mice showed a significantly greater cardiac hypertrophic response than WT mice. On the other hand, cardiac function and heart rate were similar in PMCA1Ht and WT mice. While angiotensin II had no effect on PMCA1 expression in the heart, it significantly increased PMCA1 expression in the aortas of both WT and PMCA1Ht mice. More importantly, WT mice had significantly higher PMCA1 expression level than the PMCA1Ht mice treated with the same dose of angiotensin II. This suggests that PMCA1 plays a pivotal role in Ca2+ extrusion in the vasculature and that under stressful conditions PMCA1Ht mice are less able to respond to stress through a compensatory increase in PMCA1 expression, leading to increased intracellular Ca2+ concentration, which in turn leads to increased vascular contractility and increased blood pressure. Conclusion: This work provides evidence that PMCA1 is involved in blood pressure regulation and protects against the development of hypertension and cardiac hypertrophy.

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12

Ng, Fu Liang. "The impact of the blood pressure-associated genetic locus at SLC4A7 on gene expression and intracellular pH regulation." Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/24732.

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Genome-wide association studies have revealed an association between variation at the SLC4A7 locus and blood pressure. SLC4A7 encodes the electroneutral Na+/HCO3 - co-transporter NBCn1 which regulates intracellular pH (pHi) in a range of tissues, including vascular smooth muscle and endothelium. Notably, the SLC4A7 knockout mouse has been shown to have an altered blood pressure phenotype. This thesis presents a functional study of variants at this locus in primary cultures of vascular smooth muscle and endothelial cells. There were genotype-dependent differences in DNA-nuclear protein interactions by formaldehyde-assisted isolation of regulatory elements, electrophoretic mobility shift assays and DNA pulldown assays. Subsequently, there were also genotypedependent differences in SLC4A7 expression level and NBCn1 availability at the plasma membrane. In turn, SLC4A7 genotype is associated with Na+/HCO3 --dependent steady-state pHi and recovery from intracellular acidosis. The genotypic effect on pHi regulation was independent of the calcineurin activity, or the amino acid substitution E326K resulting from a missense polymorphism. However, in the presence of Na+/H+ exchange activity, the SLC4A7 genotypic effect on net base uptake and steady-state pHi was detected only in vascular smooth muscle cells but not endothelial cells. The finding of a genotypic influence on SLC4A7 expression and pHi regulation in vascular smooth muscle cells provide an insight into the molecular mechanism underlying the association of variation at the SLC4A7 locus with blood pressure.

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13

Henker, Richard. "PNEUMATIC ARTIFICIAL HEART DRIVER PARAMETER EFFECTS ON THE RATE OF PRESSURE CHANGE ((+) DP/DT MAX)." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276466.

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The aim of the research was to investigate the effects of three parameters of the artificial heart on the (+) dP/dt max. The study was conducted using a mock circulation which was connected to an artificial heart. The data were collected using the COMDU software developed for the computer which monitors the artificial heart. Stepwise regression analysis was utilized to test the three hypotheses. Two of the null hypotheses for the study could not be rejected, as the independent variable did not significantly affect (+) dP/dt max. Although the third hypothesis was accepted, the results were not clinically significant. Limitations in the study were multicollinearity among the independent variables, small sample size, and the inability of the mock circulation to represent human responses.

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14

Loudon, Mary. "Arterial wall renin-like activity and blood pressure regulation in the rat." Thesis, University of Leicester, 1985. http://hdl.handle.net/2381/34141.

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In this study the Importance of the generation of angiotensin II within the blood vessel wall in determining the pressor response to injected renin was investigated. An injection of renin, given to rats after bilateral nephrectomy, produced a pressor response. The level of circulating renin, although initially elevated, returned to the normal range within three hours. However, the level of renin present in the aortic wall remained significantly elevated for six hours after the injection, as did the pressor response. Infusions of the angiotensin II antagonist saralasin at three and six hours after the renin injection confirmed that the pressor response was maintained by the renin-angiotensin system. An injection of renin into normal rats produced the same initial pressor response as was observed in the nephrectomised rats. However, the blood pressure subsequently returned to the pre-injection level after one hour. In the normal rats the pressor response was not related to the level of renin present within the aortic wall. It was concluded that the activity of the renin present within the blood vessel wall was more relevant to the control of blood pressure than the circulating level. However, when the kidneys were present this local action of the renin-angiotensin system was overriden by renal anti-hypertensive systems. This was not dependent on the presence of the renal medulla since the pressor response after chemical renal medullectomy was the same as that observed in the normal rats. The increase in the level of renin within the aortic wall after the injection of exogenous renin confirmed that renin can enter the walls of blood vessels from the circulation. It was concluded that this occurred by a process of passive diffusion.

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15

Stevens, Glen Harold John. "Blood Pressure Regulation During Simulated Orthostatism Prior to and Following Endurance Exercise Training." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc277914/.

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Cardiovascular responses and tolerance to an orthostatic stress were examined in eight men before and after eight months of endurance exercise training. Following training, maximal oxygen consumption and blood volume were increased, and resting heart rate reduced. Orthostatic tolerance was reduced following training in all eight subjects. It was concluded that prolonged endurance training decreased orthostatic tolerance and this decrease in tolerance appeared associated with attenuated baroreflex sensitivity and alterations in autonomic balance secondary to an increased parasympathetic tone noted with training.

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16

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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17

Wiemuth, Dominik, and n/a. "Regulation of the epithelial sodium channel (ENac) by ubiquitination." University of Otago. Department of Physiology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20061127.162243.

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The epithelial sodium channel (ENaC) is the central component of the sodium absorption pathway in epithelia. It is critical for sodium homeostasis and blood pressure control, which is demonstrated by rare genetic disorders such as Liddle�s syndrome and pseudohypoaldosteronism type I, that are associated with hyper- and hypotension, respectively. ENaC is mainly regulated by mechanisms that control the expression of active channels at the cell surface. Ubiquitin ligases of the Nedd4-like family, such as Nedd4 and Nedd4-2 decrease epithelial sodium absorption by binding to and targeting ENaC for endocytosis and degradation. This is most likely achieved by catalyzing the ubiquitination of ENaC. Conversely the serum- and glucocorticoid regulated kinase (SGK) increases ENaC activity. This effect is partly mediated by the interaction of SGK with the ubiquitin ligases Nedd4 and Nedd4-2. SGK is able to bind to both Nedd4 and Nedd4-2, however only Nedd4-2 is phosphorylated by SGK. The phosphorylation of Nedd4-2 inhibits its interaction with ENaC, thus reducing ENaC ubiquitination, thereby increasing surface expression and sodium absorption. Nedd4-like proteins interact with ENaC via their WW-domains. These domains bind PY-motifs (PPXY) present in ENaC subunits. Nedd4 and Nedd4-2 both have four highly similar WW-domains. Previous studies have shown that interaction between Nedd4 and ENaC is mainly mediated by WW-domain 3. SGK also has a PY-motif; therefore it was analyzed whether the WW-domains of Nedd4 and Nedd4-2 mediate binding to SGK. Here, it is shown that single or tandem WW-domains of Nedd4 and Nedd4-2 mediate binding to SGK and that, despite their high similarity, different WW-domains of Nedd4 and Nedd4-2 are involved. These data also suggest that WW-domains 2 and 3 of Nedd4-2 mediate the interaction with SGK in a concerted manner, and that in vitro the phosphorylation of SGK at serine residue 422 increases its affinity for the WW-domains of Nedd4-2. The stimulatory effect of SGK on ENaC activity is partly mediated via Nedd4-2 and will decrease if competition between Nedd4 and Nedd4-2 for binding to SGK occurs. Here it is shown that Nedd4 and Nedd4-2 are located in the same subcellular compartment and that they compete for binding to SGK. Besides its function in the proteasomal degradation pathway ubiquitination is involved in the regulation of membrane protein trafficking, including their endocytosis. ENaC was shown previously to be ubiquitinated. Here, we provide evidence that ENaC can be ubiquitinated differentially depending on its cellular location. Channels residing in the plasma membrane are multiubiquitinated and we suggest that this serves as an internalization signal for ENaC and a control for further trafficking. Cytosolic ENaC is mainly polyubiquitinated, and therefore probably targeted for proteasomal degradation. However, mono- and multiubiquitination of ENaC located within the cytosol is very likely to occur as well. In addition, it is shown that both proteasomal and lysosomal pathways are involved in the regulation of ENaC.

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18

Hendy, Emma Bernice. "Sites and mechanisms within the brainstem for chronic regulation of arterial blood pressure." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.528103.

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19

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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20

Brennan, Kathryn. "Maternal nutrient restriction alters renal development and blood pressure regulation of the offspring." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439999.

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21

Carr, Fiona Jane. "Investigation into genetic determinants of blood pressure regulation in a model of hypertension." Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250065.

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22

Dunlop, Diana Clare. "Calcium homeostasis and blood pressure regulation in normal and insulin-dependent diabetic pregnancy." Thesis, University of Bath, 1999. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311185.

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23

Andresen, Jean M. "Aortic Baroreceptor Reflex Control of Blood Pressure: Effect of Fitness." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc500922/.

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Aortic baroreflex (ABR) control of blood pressure was examined in 7 untrained (UT) and 8 endurance exercise trained (EET) young men. ABR control of blood pressure was determined during a steady state phenylephrine infusion to increase mean arterial pressure 10-15 mmHg, combined with positive neck pressure to counteract the increased carotid sinus transmural pressure, and low levels of lower body negative pressure to counteract the increased central venous pressure. Functioning alone, the ABR was functionally adequate to control blood pressure. However, ABR control of HR was significantly diminished in the EET subjects due solely to the decrease in the ABR sensitivity. The persistent strain from an increased stroke volume resulting from endurance exercise training could be the responsible mechanism.

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24

Baker, Nigel Richard. "Synthesis and pharmacological activity of novel quinolones, benzopyran-4-ones and fluorobenzenes as potential cardiovascular agents." Thesis, Coventry University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245099.

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25

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.

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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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Knowles, Ian David. "The role of 5-HTâ†2 receptors in central cardiovascular regulation in anaesthetized rats." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313783.

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27

Zhao, Jiexin. "Investigating the CaMKKβ signalling pathway and its role in the regulation of blood pressure." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/42781.

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Calcium/Calmodulin dependent protein kinase kinase beta (CaMKKβ) is a serine/threonine kinase involved in the Calcium/Calmodulin dependent protein kinase (CaMK) cascade. In 2005, CaMKKβ was shown to phosphorylate and activate AMP-activated protein kinase (AMPK), a master regulator of metabolism. Activation of AMPK has previously been reported to inhibit vascular smooth muscle myosin light chain (MLC) phosphorylation. The phosphorylation state of MLC in smooth muscle is known to directly control the contractility of blood vessels and the maintenance of blood pressure. This thesis describes the characterisation of the global CaMKKβ knockout (CaMKK KO) mice, as well as the investigation of CaMKKβ signalling pathways involved in blood pressure regulation using CaMKK KO mice in a model of lipopolysaccharide induced septic shock. Septic shock is a syndrome defined by persistently reduced blood pressure despite fluid resuscitation leading to multiple organ failure resulting from overwhelming infection. Using implantable telemetry probes, aortic blood pressure was recorded in age matched male wild-type (WT) and CaMKK KO mice under both basal conditions and during lipopolysaccharide induced septic shock. In mice with global deletion of CaMKKβ, basal blood pressure was found to be increased compared to their WT littermates. In addition, when treated with intraperitoneally injected bacterial lipopolysaccharide, the lack of CaMKKβ appears to confer protection against hypotension, with significantly higher blood pressure seen in CaMKK KO mice, as well as improved mobility and general physiological state, compared to WT mice. To investigate the mechanism for the increased blood pressure in CaMKK KO mice, aorta lysate MLC kinase activity and MLC phosphorylation were measured and found to be increased in lipopolysaccharide treated CaMKK KO mice compared to WT mice. In contrast to a recent independent study, no indication of altered inflammatory response was found in CaMKK KO mice compared to WT littermates following intraperitoneal lipopolysaccharide injection. Ex vivo lipopolysaccharide treatment induced similar levels of nitric oxide production and phagocytosis in primary peritoneal macrophages isolated from WT and CaMKK KO mice. In summary, CaMKKβ appears to be involved in the regulation of blood pressure. Loss of CaMKKβ in mice protects against septic shock through increased phosphorylation of MLC and the maintenance of blood pressure. Currently, septic shock is associated with a high mortality rate despite the available pharmacological treatments; inhibition of CaMKKβ could provide an alternative strategy to assist with the maintenance of blood pressure during sepsis.

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Dhindaw, Seema. "Characterization of a 793 Kilobase Segment of the Rat Genome in Blood Pressure Regulation." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1188911291.

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29

Pandey, Varunkumar Girijaprasad. "The Effect of Glucocorticoids on Regulation of the Human Angiotensinogen Gene and Blood Pressure." University of Toledo Health Science Campus / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=mco1378647891.

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30

Williams, DeWayne P. "Ethnicity, Sex, and Vagal Activity: Differences in Hemodynamics Underlying Long-Term Blood Pressure Regulation." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500640025670825.

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31

Newby, David Ernest. "Studies into the role of endogenous angiotensin II in the regulation of peripheral vascular tone in health and disease." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299605.

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32

Crandall, Craig G. (Craig Gerald). "Alterations in Human Baroreceptor Reflex Regulation of Blood Pressure Following 15 Days of Simulated Microgravity Exposure." Thesis, University of North Texas, 1993. https://digital.library.unt.edu/ark:/67531/metadc278142/.

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Prolonged exposure to microgravity is known to invoke physiological changes which predispose individuals to orthostatic intolerance upon readaptation to the earth's gravitational field. Attenuated baroreflex responsiveness has been implicated in contributing to this inability to withstand orthostatic stress. To test this hypothesis, eight individuals were exposed to 15 days of simulated microgravity exposure using the 6° head-down bed rest model. Prior to, and after the simulated microgravity exposure, the following were assessed: a) aortic baroreflex function; b) carotid baroreflex function; c) cardiopulmonary baroreflex function; and d) the degree of interaction between the cardiopulmonary and carotid baroreflexes.

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33

Hudson, Donna Louise. "The Effects of Lower Body Negative Pressure on the Cardiovascular System: The Relationships of Gender and Aerobic Fitness." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc935602/.

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Sixteen males and sixteen females were recruited for this study; eight of each gender were aerobically trained athletes; the remaining eight were untrained control subjects. Each subject performed a maximal exercise stress test for aerobic capacity (VO2max). On a separate day the blood volume and the cardiovascular responses to progressive (0 to -50 torr) lower body negative pressure (LBNP) were determined. The female subjects were observed to be significantly more tolerant of the LBNP than the male subjects. No differences between groups were observed in changes in leg volume, cardiac index, blood pressure, or heart rate during LBNP. However, the females, in comparison to the males, maintained stroke index at a higher level, and increased regional vasoconstriction more, during the LBNP induced hypotensive stress. These findings suggest that female subjects withstand LBNP to -50 torr better than male subjects.

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Pollock, Brandon S. "Determining the influence of limb and gender on blood pressure regulation and functional sympatholysis during the application of negative pressure." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1445348894.

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D'Antono, Bianca. "The relationship between risk for hypertension and the regulation of blood pressure and pain sensitivity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0024/NQ50139.pdf.

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Vasudevan, Harish. "Testosterone-dependent vascular arachidonic acid metabolism in the regulation of insulin resistance and blood pressure." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/8704.

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Insulin resistance (IR) and elevated blood pressure (BP) are two key features of the metabolic syndrome, which play an important role in the development of secondary cardiovascular complications. Feeding rats a diet rich in sugars such as fructose induces IR followed by vascular abnormalities and elevation in BP. Insulin resistance impairs the fine balance between endothelial vasoconstrictors and vasorelaxants, which results in endothelial dysfunction (ED). Differences in sex hormones play an important role in the development of insulin resistance and blood pressure as testosterone is essential for the development of ED and the increase in BP. Testosterone regulates the cyclooxygenase and Cyp4A-catalyzed metabolites of arachidonic acid, which have been implicated in vascular homeostasis. However, their regulation by insulin is unclear. We hypothesized that In the presence of testosterone insulin resistance favors increased synthesis of vasoconstrictor metabolites of arachidonic acid, which contributes to the development of endothelial dysfunction and subsequent elevation of blood pressure. Intact and/or gonadectomized male Wistar rats were fed for 9-12 weeks with fructose following which changes in blood pressures and vascular reactivity were determined. Treatment with testosterone restored the elevated blood pressure in gonadectomized rats. In addition, fructose-feeding induced insulin resistance in intact rats, which was ameliorated by inhibiting the androgen receptor or 20-HETE synthesis. Insulin resistance increased Cyp4A1, 2/3 expression in the superior mesenteric artery (SMA), which was decreased by blocking testosterone function. Finally, the increase in BP and Cyp4A1, 2/3 were prevented by treating rats for 2 weeks with the Cyp4A inhibitor HET0016. The role of IR in arachidonate metabolism was evaluated by treatment with metformin (500 mg/kg) for 10 weeks. Prevention of insulin resistance prevented both endothelial dysfunction and the increase in BP. Further, inhibition of Cyp4A by DDMS improved endothelial relaxation in the SMA of only intact and untreated FFR but not the gonadectomized and metformin-treated groups. Similar effects were observed upon blocking COX with indomethacin. IR increased the participation of COX-2, which was testosterone-dependent in both aorta and SMA. In conclusion, in the presence of testosterone, IR induces vascular complications by altering arachidonic acid metabolism to increase vasoconstrictor levels.

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Nakao, Kazuhiro. "ENDOTHELIUM-DERIVED C-TYPE NATRIURETIC PEPTIDE CONTRIBUTES TO BLOOD PRESSURE REGULATION BY MAINTAINING ENDOTHELIAL INTEGRITY." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225500.

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Ramsey, Michael W., Bradley J. Behnke, Rhonda D. Prisby, and Michael D. Delp. "Effects of Aging on Adipose Resistance Artery Vasoconstriction: Possible Implications for Orthostatic Blood Pressure Regulation." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/4135.

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The purpose of this investigation was to determine mean arterial pressure (MAP) and regional vascular conductance responses in young and aged Fisher-344 rats during orthostatic stress, i.e., 70° head-up tilt (HUT). Both groups demonstrated directionally different changes in MAP during HUT (young, 7% increase; aged, 7% decrease). Vascular conductance during HUT in young rats decreased in most tissues but largely remained unchanged in the aged animals. Based on the higher vascular conductance of white adipose tissue from aged rats during HUT, resistance arteries from white visceral fat were isolated and studied in vitro. There was diminished maximal vasoconstriction to phenylephrine and norepinephrine (NE: young, 42 ± 5%; old, 18 ± 6%) in adipose resistance arteries from aged rats. These results demonstrate that aging reduces the ability to maintain MAP during orthostatic stress, and this is associated with a diminished vasoconstriction of adipose resistance arteries. With advancing age the ability to tolerate orthostatic stress (17, 22) and perform exercise (11, 15, 34) is reduced. One possible mechanism for these age-related changes is a diminished arterial vasoconstrictor responsiveness, which could impair redistribution of cardiac output during exercise and limit reductions in vascular conductance during orthostasis. The ability to diminish vascular conductance in nonactive tissue is requisite during orthostasis to maintain mean arterial pressure (MAP) and sustain adequate brain perfusion. However, whether regional vascular conductance during orthostasis is altered by aging remains unknown. Head-up tilt (HUT) has been utilized extensively to study cardiovascular system responsiveness to orthostatic stress in humans and animals (8, 13, 14, 16, 26, 31). Postural changes from the supine position to the upright posture elicit a blood volume shift from the thoracic cavity to the lower limbs (29), which results in reduced venous return and, subsequently, decreased stroke volume. The resultant decrease in cardiac output must be offset by a decrease in peripheral vascular conductance (PVC) to maintain arterial blood pressure (29). Since there is a greater incidence of orthostatic hypotension with advancing age (16, 25, 31, 38), the primary purpose of the present study was to determine whether a diminished ability to maintain MAP during an orthostatic stress is manifest in aged Fischer-344 rats and to identify whether alterations in regional vascular conductance correspond to a putative orthostatic hypotension. Specifically, we hypothesized that with HUT, aged animals will demonstrate a diminished vasoconstriction in some tissues, as evidenced by higher blood flows and vascular conductance relative to that in young adult rats. The results indicated an inability of old rats to diminish vascular conductance in several tissues, including white adipose tissue, during HUT. Therefore, a secondary purpose was to test the hypothesis that aging diminishes myogenic and adrenergic vasoconstriction of resistance vessels from white visceral adipose tissue. The results from this series of experiments may indicate an underlying mechanism for the old age-related orthostatic intolerance. Given that adipose tissue makes up a greater proportion of body composition with aging in rats (7) and humans (1), a reduced vasoconstriction of resistance vessels from this tissue could have significant ramifications on the ability to decrease peripheral vascular conductance during orthostatic challenges and with exercise among the elderly.

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Azizi, Newsha. "Blood pressure regulation in ANP-knockout mice, the role of angiotensin II-stimulated vasopressin release mechanism." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0027/MQ40861.pdf.

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Grimaldi, Daniela <1974&gt. "Narcolepsy: state-dependent autonomic regulation and circadian control of blood pressure, heart rate, body core temperature." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2009. http://amsdottorato.unibo.it/1706/.

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Debiec, Radoslaw Marek. "Analysis of genetic variation within urotensin-II system in regulation of blood pressure and renal function." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/28017.

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Elevated blood pressure (BP) and reduced glomerular filtration rate (GFR) are risk factors for cardiovascular disease. BP and GFR are influenced by heritable factors. Only small proportion of this heritability has been explained so far. This project aimed to identify genetic loci contributing to population variation in BP or GFR through application of candidate gene and large scale genotyping approaches. The candidate gene approach utilised tagging single nucleotide polymorphisms (SNP) in genes of the urotensin-II (U-II) pathway in a sample of white European subjects (3 family collections and 5 unrelated subject studies – altogether 10,748 subjects). This was followed by gene expression studies in 2 collections of human kidneys and phylogenetic analysis of the system to examine its evolutionary conservation from fish to human. The large scale genotyping project utilised data from 50K IBC genotyping array in a cohort of families (520 pedigrees) from general population of UK. None of the 28 SNPs in U-II pathway genes was associated with BP or GFR. Gene expression levels of UTS2 and UTS2R were strongly correlated (r=0.83, p<0.0001) but renal expression was not associated with human hypertension. The phylogenetic analysis showed that strong purifying selection acting on this system in lower vertebrates was lost in primates. The large scale genotyping approach showed strong signal of association in the 5,10-methylenetetrahydrofolate reductase (NAD(P)H) gene (MTHFR) locus with clinic diastolic BP. Each minor copy (G) of rs17037388 was associated with 2.03mmHg reduction in clinic diastolic BP (p=3.01x10[superscript -06]). Gene candidate and large scale genotyping approaches performed in parallel provide useful information about genetic architecture of complex traits. The data from genetic association in candidate U-II system genes did not provide evidence on its association with BP or GFR. Large scale genotyping experiment led to identification of genuine association signal with clinic diastolic BP.

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Adlam, David. "The role of nitric oxide - redox signalling in blood pressure and heart rate regulation in vivo." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437387.

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Ehret, Georg B., Teresa Ferreira, Daniel I. Chasman, Anne U. Jackson, Ellen M. Schmidt, Toby Johnson, Gudmar Thorleifsson, et al. "The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals." NATURE PUBLISHING GROUP, 2016. http://hdl.handle.net/10150/623255.

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To dissect the genetic architecture of blood pressure and assess effects on target organ damage, we analyzed 128,272 SNPs from targeted and genome-wide arrays in 201,529 individuals of European ancestry, and genotypes from an additional 140,886 individuals were used for validation. We identified 66 blood pressure-associated loci, of which 17 were new; 15 harbored multiple distinct association signals. The 66 index SNPs were enriched for cis-regulatory elements, particularly in vascular endothelial cells, consistent with a primary role in blood pressure control through modulation of vascular tone across multiple tissues. The 66 index SNPs combined in a risk score showed comparable effects in 64,421 individuals of non-European descent. The 66-SNP blood pressure risk score was significantly associated with target organ damage in multiple tissues but with minor effects in the kidney. Our findings expand current knowledge of blood pressure-related pathways and highlight tissues beyond the classical renal system in blood pressure regulation.

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Ibeawuchi, Stella-Rita C. "Regulation of vascular function: roles for Cullin-3 and RhoBTB1 In Pparγ-mediated blood pressure control." Diss., University of Iowa, 2015. https://ir.uiowa.edu/etd/1637.

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Hypertension and type II diabetes are key components of metabolic syndrome affecting one third of US population. Insulin-sensitizing thiazolidinediones (TZDs) are high affinity synthetic ligands for Peroxisome Proliferator-Activated Receptor gamma (PPARG), a nuclear receptor and ligand-activated transcription factor. Clinical data show that TZDs are cardioprotective and lower blood pressure even with increased water and salt retention, suggesting a direct role for PPARG in blood pressure regulation. Human subjects with PPARG mutations exhibit severe early onset hypertension, insulin resistance and type II diabetes. These PPARG mutations, V290M and P467L, affect the ligand-binding domain of PPARG and have dominant negative effect on transcriptional activity. However, the mechanism by which PPARG regulates blood pressure remains elusive. A common feature of hypertension is increased RhoA activity and transgenic mice expressing dominant negative PPARG in vascular smooth muscle cells (S-P467L) exhibit hypertension and severe aortic dysfunction dependent on over-activation of the RhoA/ROCK signaling. Previously published data from our group report that smooth muscle-specific interference of PPARG impairs Cullin-3 E3 ubiquitin ligase-mediated regulation of RhoA and identify Cullin-3 as a novel regulator of vascular function. Patients with de novo mutations that lead to deletion of 57 amino acids encoded by exon 9 in Cullin-3 have early onset hypertension, but the mechanistic basis for this effect is lacking. We show that Cul3 mutation resulted in reduced RhoA ubiquitination and degradation. Reduced Cullin-3 activity increases the RhoA pool that can be activated to a GTP bound state by cellular RhoGEFs in response to contractile agonists promoting hypertension. We have identified a novel PPARG target gene-RhoBTB1, a component of the Cullin-3 RING E3 ubiquitin ligase (CRL3) complex. SiRNA-mediated knockdown of RhoBTB1 significantly decreased Cul3 protein levels resulting in a modest increase in RhoA protein. To understand the fundamental mechanisms by which vascular PPARG regulate vascular function, we generated a transgenic mice with smooth muscle-specific overexpression of RhoBTB1 (S-RhoBTB1) and crossed with the S-P467L mice. We show that replacement of RhoBTB1 in the vascular smooth muscle complements the defects observed in S-P467L due to PPARG interference. This study will advance our understanding on how PPARG regulates blood pressure so that new therapies that maximize the beneficial effects of PPARG can be developed.

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Turnbull, Fiona. "Effects of different blood pressure-lowering regimens on major cardiovascular events in major patient subgroups." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28142.

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Background Cardiovascular disease is a leading cause of mortality and morbidity worldwide. Blood pressure is the single, most important risk factor for cardiovascular disease; nearly two-thirds of all strokes and approximately half of all ischaemic heart disease events are attributable to non-optimal blood pressure. The evidence from individual randomised trials of blood pressure lowering regimens suggests that that protection from major cardiovascular events can be achieved by lowering blood pressure, even among those with so-called ‘normal’ blood pressures. However, many trials are not sufficiently powered to demonstrate modest but clinically important differences in the effects of different classes of drug on the risk of cardiovascular disease. As a result, there is considerable uncertainty about the relative effectiveness of different drug classes. Reliable and precise information about the effects of treatment is central to the management of cardiovascular risk in millions of people worldwide. The aim of the research contributing to this thesis was to generate high quality evidence about the effects of a range of blood pressure lowering regimens on major cardiovascular outcomes in important patient subgroups. Methods The research uses prospectively-planned overviews (meta-analyses) of large randomised trials to generate precise estimates of treatment effect. The trials contributing to the overviews were those participating in the Blood Pressure Lowering Treatment Trialists’ Collaboration. Data from all relevant trials were submitted to the Collaboration Secretariat based at the George Institute for International Health in Sydney, Australia for inclusion in analyses. Data were combined using standard meta-analytic techniques and reported as pooled point estimates and 95% confidence intervals for the six pre-specified primary outcomes of stroke, coronary heart disease, heart failure, cardiovascular death and total mortality. The analyses comprised three main components: (1) one main set of overview analyses to examine treatment effects in the overall study population; (2) three sets of overview analyses to examine treatment effects in subgroups of younger and older patients, men and women and patients with and without diabetes; and (3) a series of post-hoc analyses (meta-analysis and meta-regression analysis) to examine the relative contributions of blood pressure-dependent and independent effects of two main classes of blood pressure drugs, ACE-I inhibitors and angiotensin receptor blockers.

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Van, Berge-Landry Helene Margaret-Rose. "Ethnic differences in diurnal blood pressure variation and regulation the effects of catecholamines, cortisol, and IL-6 /." Diss., Online access via UMI:, 2008.

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Crossley, II Dane Alan. "The Role of Pulmocutaneous Baroreceptors in the Control of Lymphatic Heart Rate in the Toad Bufo Marinus." PDXScholar, 1995. https://pdxscholar.library.pdx.edu/open_access_etds/4892.

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The present study documents that baroreceptors located in the pulmocutaneous artery (PCA) are key components in control of lymph heart rate in amphibians. A negative feedback control loop exists between arterial pressure and lymphatic heart rate. The recurrent laryngeal nerve (rLN), which innervates the PCA baroreceptors, transmits information on arterial pressure to integration centers in the central nervous system. Lymphatic heart rate (LHR) is reduced as a result of increases in arterial pressure. This loop was determined using three experimental protocols. First, the correlation between LHR reduction and hormonally induced vasoconstriction was determined. Increases in arterial pressure due to pressor actions of angiotensin II and arginine vasotocin at high concentrations was negatively correlated to LHR. Second, lymphatic heart rate changes due to natural increases in arterial pressure were compared to rate changes due to increase in arterial pressure after bilateral denervation of the rLN. Post-denervation LHR was not affected by natural increase in arterial pressure prior to the establishment of a new resting arterial pressure. Increase in arterial pressure due to administration of vasoconstricting hormones was negatively correlated with LHR following denervation. Third, the effect on LHR due to direct stimulation of the rLN was studied. Stimulation of the rLN caused LHR to stop without increases in arterial pressure. Presumably, this negative feedback loop is present to limit fluid return to the cardiovascular system from the lymphatic system during periods of acute hypertension. Reduction in the return of lymph volume to the cardiovascular system could eliminate potential damage to pulmonary tissues due to high arterial pressures.

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Smith, Michael Lamar 1957. "Fitness-Related Alterations in Blood Pressure Control: The Role of the Autonomic Nervous System." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc331614/.

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Baroreflex function and cardiovascular responses to lower body negative pressure during selective autonomic blockade were evaluated in endurance exercise trained (ET) and untrained (UT) men. Baroreflex function was evaluated using a progressive intravenous infusion of phenylephrine HCL (PE) to a maximum of 0.12 mg/min. Heart rate, arterial blood pressure, cardiac output and forearm blood flow were measured at each infusion rate of PE. The reduction in forearm blood flow and concomitant rise in forearm vascular resistance was the same for each subject group. However, the heart rate decreases per unit increase of systolic or mean blood pressure were significantly (P<.05) less in the ET subjects (0.91 ± 0.30 versus 1.62 ± 0.28 for UT). During progressive lower body negative pressure with no drug intervention, the ET subjects had a significantly (P<.05) greater fall in systolic blood pressure (33.8 ± 4.8 torr versus 16.7 ± 3.9 torr). However, the change in forearm blood flow or resistance was not significantly different between groups. Blockade of parasympathetic receptors with atropine (0.04 mg/kg) eliminated the differences in response to lower body negative pressure. Blockade of cardiac sympathetic receptors with metoprolol (0.02 mg/kg) did not affect the differences observed during the control test. It was concluded that the ET subjects were less effective in regulating blood pressure than the UT subjects, because of 1) an attenuated baroreflex sensitivity, and 2) parasympathetic-mediated depression of cardiac and vasoconstrictive responses to the hypotensive stress.

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Czopek, Alicja. "Effect of maternal iron deficiency during pregnancy on kidney development and blood pressure regulation in the rat offspring." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=26459.

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Puvi-Rajasingham, Sharmini. "Interrelation of mechanical neural and hormonal factors in the regulation of superior mesenteric artery blood flow and systemic blood pressure in normal and abnormal man." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298190.

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Dissertations / Theses on the topic 'Blood pressure regulation'

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