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1
Kirk, Jane Elizabeth. "Pharmacological manipulation of natriuretic peptides." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244588.
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Willeit, Peter. "Natriuretic peptides and cardiovascular disease." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648533.
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Sharma, Vishal. "Natriuretic peptides in valvular heart disease." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23463.
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Plasma natriuretic peptide concentrations rise in response to either atrial or ventricular wall stretch and have been found to be useful in the diagnosis and assessment of patients with congestive cardiac failure. Although previous studies have suggested that plasma natriuretic peptides may offer some prognostic information in patients with valvular heart disease, it is unclear whether concentrations reflect disease severity and how plasma concentrations vary across different valve lesions. The aim of this research was to identify the factors that affect natriuretic peptide releases in valvular heart disease (VHD) and to investigate whether natriuretic peptides can be used in clinical practice to identify those patients who may benefit from early intervention. Plasma brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) concentrations were measured in patients with normal left ventricular (LV) systolic function and isolated VHD (mitral regurgitation, MR, n=33; aortic regurgitation, AR, n=39; aortic stenosis, AS, n=34; mitral stenosis, MS, n=30), and age and sex matched controls (n=39) immediately prior to exercise stress echocardiography. Peptide levels were compared against age and sex matched controls and against markers of severity for each valve lesions and across different valve lesions. Compared to controls, patients with all types of VHD had elevated plasma BNP concentrations [(MR median 35(inter quartile range 23-52), AR 34(22-45), AS 31(22-60), MS 58(34-90); controls 24(16-33) pg/mL; p < 0.01 for all]. LV end diastolic volume index varied by valve lesion; [MR (mean ± standard deviation 77±14), AR (91±28), AS (50±17), MS (43±11), controls (52±13) mL/m2; p < 0.0001]. There were no associations between LV volume and BNP. Left atrial (LA) area index varied [MR (18±4cm2/m2), AR (12±2), AS (11±3), MS (19±6), controls (11±2); p < 0.0001], but correlated with plasma BNP concentrations: MR (r=0.42,p=0.02), MS (r=0.86,p < 0.0001), AR (r=0.53,p=0.001), AS (r=0.52, p=0.002). Higher plasma BNP concentrations were associated with increased pulmonary artery pressure and reduced exercise capacity. Despite adverse cardiac remodelling, 81(60%) patients had a BNP concentration within the normal range. In patients with MS BNP was strongly associated with left atrial area index (r=0.86; p < 0.0001) and a BNP level of greater than 2 times the upper limit of normal identified patients who fulfilled guideline criteria for intervention (Area under the curve (AUC) 0.87 [0.74,0.99], p =0.006) and lower exercise capacity (AUC 0.82 [0.67,0.97]; p=0.004). In AR patients significant remodelling could occur whilst BNP remained within the normal range and in general BNP appeared less useful in assessing disease severity. However raised levels of BNP was associated with more severe AR as assessed by left ventricular outflow tract:AR Jet area ratio (r=0.43 p=0.0007). AR patients with an abnormal BNP had signs of early LV dysfunction on exercise with a lower LV longitudinal strain rate post exercise compared to AR patients with a normal BNP (0.68±0.31 vs. 1.06±0.45 1/sec; p=0.02). In MR patients, higher plasma BNP concentrations were associated with larger left atrial area index (r=0.42, p=0.02), higher pulmonary artery pressure (r=0.53, p=0.002) and a lower exercise time (r=-0.60, p=0.0002). BNP was not associated with any marker of left ventricular size or function in MR. These findings suggest that despite significant LV remodelling, plasma BNP concentrations are often normal in patients with VHD. Consequently, plasma BNP concentrations should be interpreted with caution when assessing patients with VHD. However natriuretic peptide levels offer complementary information to the standard assessment of patients with VHD and an unexplained finding of an elevated BNP in an otherwise asymptomatic patient should prompt further investigation.
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Fowkes, Robert Charles. "Natriuretic peptides in the pituitary : expression, action and regulation of C-type natriuretic peptide (CNP) in gonadotrophs." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246294.
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Ruzvidzo, Oziniel. "Plant Natriuretic Peptides - Elucidation of the Mechanisms of Action." Thesis, University of the Western Cape, 2009. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_5854_1285860491.
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Several lines of cellular and physiological evidence have suggested the presence of a novel class of systemically mobile plant molecules that are recognized by antibodies generated against vertebrate atrial natriuretic peptides (ANPs). Functional characterization of these immunoanalogues, referred to as immunoreactive plant natriuretic peptides (irPNPs) or plant natriuretic peptides (PNPs), has shown that they play important roles in a number of cellular processes crucial for plant growth and maintenance of cellular homeostasis. Although the various biological roles of PNPs in plants are known, their exact mode of action remains elusive. To elucidate the mechanisms of action for these immunoanalogues, we have prepared a biologically active recombinant PNP from Arabidopsis thaliana (AtPNP-A) and the biological activity was demonstrated by showing its ability to induce water uptake into Arabidopsis thaliana protoplasts. In addition, the molecule was shown to downregulate photosynthesis while at the same time up-regulating respiration, transpiration as well as net water uptake and retention capacities in the sage Plectranthus ecklonii. Further analysis of the recombinant AtPNP-A indicated that the peptide can induce systemic response signalling though the phloem. A recombinant Arabidopsis wall associated kinase-like protein (AtWAKL10) that has a domain organization resembling that of vertebrate natriuretic peptide (NP) receptors was also partially characterized as a possible receptor for the recombinant AtPNP-A. Vertebrate NP receptors contain an extracellular ligand-binding domain and an intracellular guanylate cyclase (GC)/kinase domain and signal through the activity of their GC domain that is capable of generating intracellular cGMP from GTP. The structural resemblance of AtWAKL10 to vertebrate NP receptors could suggest a functional homology with receptor molecules and it is conceivable that such a receptor may recognize PNPs as ligands. The characterization of the recombinant AtWAKL10 showed that the molecule functions as both a GC and a kinase in vitro. This strengthened the suggestion that AtWAKL10 could be a possible AtPNP-A receptor especially considering the fact that AtPNP-A applications to plant cells also
trigger cGMP transients. Furthermore, a bioinformatic analysis of the functions of AtPNP-A and AtWAKL10 has inferred both molecules in plant pathogen responses and defense mechanisms, thus indirectly functionally linking the two proteins.
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Hove, Runyararo Memory. "Evolutionary development and functional role of plant natriuretic peptide (PNP)-B." Thesis, University of Fort Hare, 2009. http://hdl.handle.net/10353/155.
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Plant natriuretic peptides (PNP) are novel peptides which, like in vertebrates, have been shown to have a function associated with water and salt homeostasis. Two PNP-encoding genes have been identified and isolated from Arabidopsis thaliana, namely; AtPNP-A and AtPNP-B. In this study, the focus was on PNP-B, which has not been extensively studied. Bioinformatic analysis was done on the AtPNP-B gene. This included the bioinformatic study of its primary structure, secondary structure, tertiary structure, transcription factor binding sites (TFBS) and its relation to other known proteins. The AtPNP-B gene was shown to be a 510 bp long, including a predicted 138 bp intron. AtPNP-B was also shown to have some sequence similarity with AtPNP-A and CjBAp12. The TFBS for AtPNP-B and OsJPNP-B were compared and they comprised of TFBS that are related to water homeostasis and pathogenesis. This suggested two possible functions; water stress and homeostasis and a pathogenesis related function for PNP-B. Following bioinformatic analysis, the heterologous expression of the AtPNP-B was attempted to investigate whether the AtPNP-B gene encoded a functional protein and to determine the functional role of PNP-B. However, expression was unsuccessful. An evolutionary study was then carried out which revealed that there were some plants without the intron such as, rice, leafy spurge, oilseed rape, onion, poplar, sugar cane, sunflower and tobacco. These plants would therefore be used for expression and functional studies in the future. The evolutionary studies also revealed that PNP-B had a relationship with expansins and the endoglucanase family 45. Other PNP-B related molecules were also obtained from other plant genomes and therefore used in the construction of a phylogenetic tree. The phylogenetic tree revealed that AtPNP-B clustered in the same group as CjBAp12 while AtPNP-A had its own cluster group. There were also other PNP-B like molecules that clustered in the same group as expansins (α- and β-). Thus, we postulate that, like PNP-A, PNP-B also has a possible function in water and salt homeostasis. However, due to the clustering iii of AtPNP-B into the same group as CjBAp12, a possible role of PNP-B in pathogenesis-related response is also postulated.
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Thomas, Colleen J(Colleen Joy) 1965. "Influence of natriuretic peptides on cardiac reflexes." Monash University, Dept. of Physiology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8347.
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Woodard, Geoffrey Esty. "Non-cardiac natriuretic peptides in the rat." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621143.
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Vries, Petrus Johannus Fransciscus de. "Atrial natriuretic peptides their role in cardiovascular homeostasis /." Maastricht : Maastricht : Datawyse ; University Library, Maastricht University [Host], 1990. http://arno.unimaas.nl/show.cgi?fid=6192.
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Kao, Jonathan. "Atrial natriuretic peptide in aging rats : evidence for altered processing, secretion and receptor binding." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28993.
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The recently discovered atrial natriuretic peptide (ANP) has potent diuretic, natriuretic and hypotensive effects, and is believed to be involved in the maintenance of sodium homeostasis in both normal and pathological conditions. The mammalian aging process is associated with a host of abnormalities that include, among others, a compromised ability to regulate sodium homeostasis. There are reports that demonstrate a positive correlation between plasma ANP levels and age in man; accordingly, the aim of this study was to examine whether age-related sodium imbalance is associated with disturbances in the homeostasis of ANP. Specifically, the intracellular storage, processing and secretion of ANP from the atrium was studied and associated with circulating ANP concentrations and ANP receptor binding kinetics.
Studies were conducted with four groups of male Wistar rats designated as 1-, 3-, 10-, and 20-month-old. 24-hour renal clearances were conducted to assess age-related changes in renal functions. GFR and UNaV increased steadily from 1 to 10 months of age and decreased in the 20-month-old, while fractional excretion of water (FEH₂O) and sodium (FENa) declined initially (from 1 to 10 months) and then rose in the 20-month-old group.
Circulating ANP levels in the rats was significantly correlated with the increase in age (N = 147, r = 0.59, p < 0.0005). Atria of the animals were isolated and superfused with a modified Langendorff apparatus. The spontaneous release of ANP increased from 1 to 3 months, and steadily decreased after 3 months. The results indicate that ANP secretion increases with maturation and thereafter declines with advancing age.
ANP concentrations in the right and left atria were also quantified. The results revealed that atrial ANP content increased from 1 to 3 months and decreased progressively with age. There was a positive correlation between the rate of ANP release and atrial ANP content (N= 42, r=0.50, p<0.01), suggesting that the release of ANP from the right atrium was associated with the atrial content. The concurrence of a reduction in ANP secretion but with elevation in plasma ANP concentration in the aged (20-month-old) rats, suggests that there may be an impairment in renal clearance of ANP.
It was established that the main molecular species present in the atrium was γ-ANP and that this was unaffected by age as assessed by reverse-phase high performance liquid chromatography (RP-HPLC) coupled with radioimmunoassay. The molecular forms of ANP secreted by the atrium consisted of predominantly α-ANP, with a smaller amounts of γ-ANP. γ-ANP constituted only 1% of the total secreted ANP in the 1-, 3-, or 10-month-old rats, but up to 8% was detected in 20-month-old rats. Although both α-ANP and γ-ANP were present in the circulation, the ratio of γ-ANP/α-ANP increased significantly with age. The concentration of γ-ANP in the plasma of the 20-month-old rats was two- to three-fold higher than in the two younger groups (1- and 3-month-old). These data imply that the post-transcriptional processing of prohormone γ-ANP to active α-ANP is altered with age.
Radio-ligand binding experiments were carried out using glomerular ANP receptors to determine whether the age-related alterations in plasma ANP levels has an effect on the binding of ANP to its target tissues. Both the receptor density (Bmax) and the equilibrium dissociation constant (kd increased from 1 to 3 months but decreased from 3 to 20 months.
Collectively, these results suggest that:
1) Aging affects atrial ANP content and consequently influences the release of ANP from the isolated atria.
2) The processing of prohormone γ-ANP to active α-ANP is modified with age.
3) Plasma levels of ANP increase with age, which may result in down-regulation of ANP receptor density and increased efficacy in receptor binding affinity. These may represent the compensatory responses.Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
11
Zuo, Zhi-Yi. "Receptors of C-type natriuretic peptides in the rat." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627660.
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Kalra, Paul Raj. "Natriuretic peptides and metabolic pathways in chronic heart failure." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503841.
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Mistry, Sanjay. "Differential expression of natriuretic peptide receptors in primary cultures of rat and human proximal tubular cells : a role for the natriuretic peptides." Thesis, University of Aberdeen, 1998. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU100279.
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The natriuretic peptide system consists primarily of the peptides, atrial natriuretic factor (ANF), brain natriuretic peptide (BNP) and c-type natriuretic peptide (CNP) and their actions are mediated via the natriuretic peptide receptors -A, -B and -C (NPR-A, -B, -C). Collectively, these peptides and receptors form an integrated hormonal system, which acts to regulate body fluid homeostasis and blood pressure control. This thesis aimed to confirm natriuretic peptide and NPR expression in freshly isolated and primary cultures of both rat and human proximal tubular (PT) cells, and to identify a possible role for local natriuretic peptide production. Local expression and production of the natriuretic peptides and NPRs was confirmed by RT-PCR, Northern analysis, cGMP response to ANF (NPR-A) and CNP (NPR-B) and RIA for the peptides A, B and C. This study demonstrated that PT cells in culture express both natriuretic peptides and NPRs, and that the process of culture results in increased natriuretic peptide expression and secretion. Furthermore, growth in culture results in a shift in NPR expression from the NPR-C in freshly isolated cells to the functional GC-linked NPR-A and -B at confleunce. Short-term incubation with exogenous natriuretic peptides suggested that natriuretic peptides could accelerate or induce changes in natriuretic peptide and NPR subtype expression, possibly via the NPR-C. The differential expression and secretion of natriuretic peptides and NPRs at different stages of culture strongly suggests a growth modulatory role for the natriuretic peptide system. These growth modulatory actions appear to be mediated by the NPR-C during the initial stages of culture and by the GC-linked NPR at later stages in culture. These results add further strength to the hypothesis that the natriuretic peptides and both the GC-linked NPR and the NPR-C, once thought to be a 'quiescent' receptor, act to modulate cell growth.
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Zhang, Jin. "Inhibition of pulsatile luteinizing hormone release by atrial natriuretic peptide and brain natriuretic peptide in the ovariectomized rat." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29412.
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Atrial natriuretic peptide (ANP) of atrial myocyte origin, has been shown to play a role in the diuresis, natriuresis, and antagonism of angiotensin and vasopressin. However, it is now apparent that in addition to the production of the peptide in the heart and in its role in fluid and electrolyte homeostasis, it is also produced in the central nervous system participating in the regulation of pituitary hormone secretion. Administration of ANP through both central and peripheral routes has been shown to inhibit secretion of luteinizing hormone (LH) in the gonadectomized rat model. A better understanding of the modulatory role of ANP on LH secretion and its possible mechanisms will add to our knowledge of the effects of neuropeptides on reproductive function.
Brain natriuretic peptide (BNP) is a bioactive peptide of 26 amino acid residues recently identified in porcine brain. The peptide exerts potent diuretic-natriuretic and vasorelaxant effects, in a manner similar to that of ANP. BNP has a remarkable high sequence homology to ANP, especially in the 17 amino acid ring formed by an intramolecular disulfide linkage which is required for biological activity. The
presence of BNP with ANP in the mammalian brain and remarkable resemblance in their molecular structures and physiological functions implies that BNP may also exert an inhibitory effect on LH secretion like ANP.
This research focused on the effects of centrally administered ANP and BNP on pulsatile LH secretion and their possible mechanisms of action in ovariectomized rats. After third ventricle infusion of ANP or BNP, inhibition of mean plasma LH level, LH pulse amplitude and pulse frequency was observed.
In searching for the possible mechanisms of inhibitory effect of ANP or BNP on pulsatile LH secretion, the effect of inhibiting the endogenous opiate system with naloxone on the action of centrally administered ANP or BNP was tested. Application of naloxone reversed the inhibitory effect of ANP and BNP on mean plasma LH level and LH pulse amplitude, but in terms of pulse frequency, naloxone treatment failed to reverse the inhibitory effect of ANP or BNP.
In separate experiments, pretreatment with pimozide, a dopaminergic receptor blocker, prevented the inhibitory action of ANP and BNP on LH secretion. After infusion of ANP or BNP, there were no significant decrease in mean plasma LH level, pulse amplitude and pulse frequency in the pimozide-pretreated
rats.
In summary, the present study shows that both ANP and BNP inhibit pulsatile LH secretion, suggesting that the inhibitory effects on LH secretion once thought to be mediated by ANP alone may be regulated through a dual mechanism involving both ANP and BNP. Furthermore, the inhibitory mechanisms may involve the interactions of ANP and BNP with central opiate system and dopaminergic system on LH secretion.Medicine, Faculty of
Obstetrics and Gynaecology, Department of
Graduate
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Majalahti, T. (Theresa). "Mechanisms of cardiac chamber-specific gene expression of natriuretic peptides." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289002.
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Abstract
Clarification of the mechanisms of cardiac-specific gene expression provides not only basic knowledge about how the gene expression is regulated in the heart, but also about the changes in the gene expression during the development of cardiovascular diseases. The purpose of this study was to analyze the mechanisms of cardiac chamber-specific gene expression and cardiac gene activation induced by mechanical load.
In the present study, the experiments were carried out by using two cardiac genes, salmon cardiac peptide (sCP) and rat B-type natriuretic peptide (BNP) genes as models. sCP was discovered previously in our laboratory and turned out to be extremely cardiac-specific, representing A-type natriuretic peptide characters in an exaggerated way. In neonatal rat cardiomyocytes, the sCP promoter activity was shown to be strictly restricted to atrial cells and the promoter to be inert to cardiac hypertrophy-inducing factors. In order to find out the mechanisms of earlier proved BNP gene activation by mechanical load, BNP promoter activity was studied in vivo in adult rat hearts. The tandem GATA transcription factor binding site at position -80/-91 was shown to be essential for the BNP gene induction by angiotensin II. To clarify the possiblity to transfer the characters of the BNP gene into the sCP gene, short BNP fragments were inserted to the sCP gene promoter. The otherwise atrial-restricted sCP promoter was shown to be switched on in rat ventricular cardiomyocytes by adding a short BNP proximal promoter element to the sCP promoter, preferably near to the transcription start site. This activity was partly dependent on the -80/-91 GATA sites in the BNP promoter. Thus, A-type natriuretic peptide regulation can be switched to B-type regulation by a short proximal BNP promoter element. In conclusion, these studies reveal certain basic differences in cardiac atrial and ventricular gene expression.
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Rugg, Elizabeth Louise. "Biochemical actions and degradations of atrial natriuretic peptide in rat tissues." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/14453.
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Atrial natriuretic peptide (ANP) has previously been shown to increase intracellular cGMP levels in isolated rat ventricular myocytes. Using purified rat cardiac sarcolemmal membranes, a series of experiments was performed to investigate the mechanisms by which this occurs. A second series of experiments was carried out to investigate the nature of ANP degradation by preparations isolated from rat heart, lung and kidney. In rat cardiac sarcolemmal membranes, ANP produced a 1.8-fold stimulation of manganese-dependent guanylate cyclase activity, with a Km of around 1nM. This activity was attenuated by the presence of 1 nM ATP in the incubation. In the presence of magnesium, guanylate cyclase activity was reduced 20- to 40-fold, but was augmented by ATP. Similar results were obtained in the presence of ANP-PNP, a non-hydrolysable analogue of ATP. [125I]-ANP binding studies indicated the presence of two receptor/affinity states, with KD'S of less than 10 pM, and around 1 nM for the high and low affinity sites respectively. More than 90% of these receptors were of the low affinity form. Similar results were obtained with bovine adrenal cortex membranes, but with MDCK cell membranes, only high affinity binding sites could be detected. These experiments indicate that rat cardiac sarcolemmal membranes possess ANP receptors, at least a proportion of which are coupled to guanylate cyclase. Incubation of [125I]-ANP with isolated rat ventricular myocytes, or with a cytosolic fraction prepared from these cells, resulted in its rapid degradation. The proteolytic activity appeared to be due to the action of a soluble metallopeptidase. Incubation of [125I]-ANP with a cytosolic fraction prepared from rat kidney and lung indicated that similar degradative activity could be isolated from these tissues.
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Bastian, René. "Characterisation of AtPNP-A - a novel arabidopsis thaliana gene with role in water and salt homeostasis." Thesis, University of the Western Cape, 2009. http://hdl.handle.net/11394/2818.
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Philosophiae Doctor - PhDPlant natriuretic peptides (PNPs) are a novel class of extracellular, systemically mobile molecules that elicit a number of plant responses important in homeostasis and growth. Natriuretic peptides were first identified in vertebrates where they play a role in the regulation of salt and water balance. Subsequent experimental investigations have identified the presence of a natriuretic peptide hormone system in plants. While PNPs have been implicated in various physiological responses such as stomatal guard cell movements and regulation of net water uptake, its biological role has remained elusive. Here we have used co-expression and promoter content analysis tools to understand the biological role of the Arabidopsis thaliana PNP (AtPNP-A). The analysis of AtPNP-A and its co-expressed genes revealed that genes annotated as part of the systemic acquired resistance (SAR) pathway were over-represented, thus suggesting that AtPNP-A may function as a component of plant defense responses and specifically, SAR. The results further show that AtPNP-A shares many characteristics with pathogenesis related (PR) proteins in that its transcription is strongly induced in response to pathogen challenges, thus implying a newly described role for AtPNP-A in pathogen attack. Additional tissue expression analysis also indicated distinct localization of PNP activity in sepals and transcriptional meta-analysis showed that AtPNP-A may play a role in starch breakdown. Therefore, together with the finding that AtPNP-A plays a role in regulating phloem transport, we also hypothesize that AtPNP-A may play a role in phloem unloading in sepals to assist processes such as seed formation in plants. In plants, the second messenger, guanosine 3’,5’-cyclic monophosphate (cGMP) mediates a whole range of important processes including salinity tolerance, disease resistance, drought tolerance and responses to light. Since PNPs regulate water and salt homeostasis via a cGMP-dependent signaling pathways, it is thus important to analyse the transcriptome induced by the second messenger (cGMP) in Arabidopsis thaliana to give a better understanding of its mechanism of action. This study was also supplemented by the analysis of the gibberellic acid (GA) dependent transcriptome, since cGMP also plays a role its transcription pathway. This data analysis, together with promoter content investigation, revealed that genes upregulated after cGMP treatment and down-regulated in the GA insensitive mutant (ga1-3) were enriched with a GA response element (GARE), while no GARE enrichment were observed in genes up-regulated in the ga1-3 mutant. These findings suggest that GARE is indicative of GA-induced and cGMP-dependent transcriptional up-regulation. Gene ontology analysis confirmed previous reports that cGMP is involved in ion homeostasis and indicated that the transcriptional cGMP response is bi-polar in the sense that both genes up- and down-regulated in response to cGMP is involved in cation transport. Additionally, ab initio analysis of genes transcriptionally dependent on cGMP identified CHX8 as a hub gene and promoter content of CHX8 co-expressed genes show enrichment of the GARE motif. The fact that CHX8 has its highest expression levels during male gametogenesis and pollen tube growth, together with our findings, suggest that GA-induced and cGMP- dependent genes may play a key role in ion and water homeostasis in the male gametophyte. Finally, we propose that the type of analysis undertaken here can yield new insights into gene regulation networks and inform experimental strategies to unravel complex transcription regulatory systems under different developmental and stimulus specific conditions.
South Africa
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楊鐸輝 and Tok-fai Vincent Yeung. "Aspects of the biological interactions between natriuretic peptides and cultured glial cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31981665.
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Yeung, Tok-fai Vincent. "Aspects of the biological interactions between natriuretic peptides and cultured glial cells." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18650302.
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Demerath, Theo [Verfasser], and Frank [Akademischer Betreuer] Schweda. "Natriuretic peptides buffer renin-dependent hypertension / Theo Demerath. Betreuer: Frank Schweda." Regensburg : Universitätsbibliothek Regensburg, 2015. http://d-nb.info/1074285948/34.
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Zhang, Yi. "Implications of natriuretic peptides and endothelin-1 release during myocardial ischaemia." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phz6334.pdf.
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Addenda and corrigenda are tipped-in & numbered leaves 281-282. Copies of author's previously published articles are inserted back end paper. Bibliography: leaves 222-279. Studies were performed in the Langendorff-perfused isolated rat heart, using a paradigm in which atrial distension was prevented. The release of natriuretic peptides and endothelin-1, along with cardiac function was monitored during periods of transient ischaemia or hypoxia. Additional studies were performed in patients undergoing cardiac catheterization.
22
Fan, Xiaohui. "Uroguanylin : molecular cloning and characterization of a potential natriuretic hormone /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841285.
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Man, Bik-ling. "Plasma brain natriuretic peptide and systemic ventricular function after the Fontan procedure /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B34865822.
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Ye, Xiadi. "Genetic analysis of natriuretic peptides and blood pressure in the spontaneously hypertensive rat /." [St. Lucia, Qld.], 2000. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16801.pdf.
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Ceresiani, Monica. "Ruolo dell'insulina nella regolazione dell'attività dei peptidi natriuretici cardiaci tramite i loro recettori." Doctoral thesis, Università Politecnica delle Marche, 2016. http://hdl.handle.net/11566/242474.
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Il Sistema dei peptidi natriuretici (NP) regola il metabolismo lipidico del tessuto adiposo attraverso la lipolisi e il programma termogenico. La risposta degli NP è mediata dal recettore biologicamente attivo NPRA e dal recettore di clearance NPRC ed il loro reciproco rapporto ne determina gli effetti finali. Il sistema lipolitico degli NP è notoriamente contrapposto a quello lipogenico dell’insulina. Lo scopo dello studio è stato di valutare la regolazione insulino-mediata dei recettori degli NP negli adipociti umani e determinare l’associazione tra l’espressione genica dei recettori degli NP nel tessuto adiposo viscerale (VAT) ed il profilo metabolico di pazienti sottoposti a nefrectomia. Gli adipociti differenziati (linea cellulare SGBS e VAT) sono stati trattati con insulina (100nM), con o senza pretrattamento con wortmannina (100nM), inibitore della PI3Kinasi, enzima chiave nel segnale dell’insulina, coinvolto nella via di inibizione della lipolisi negli adipociti. Ulteriori esperimenti sono stati effettuati utilizzando un terreno con bassa concentrazione di glucosio. Negli adipociti è stata osservata una potente up-regolazione dell’NPRC, ma non dell’NPRA, insulino-mediata e glucosio-dipendente, via PI3K. Ciò potrebbe causare una riduzione dei livelli circolanti degli NP e quindi diminuire gli effetti metabolici positivi degli NP sugli adipociti. Inoltre, si è riscontrato che il terreno con una bassa concentrazione di glucosio ostacola l'effetto dell'insulina. Nei pazienti, il rapporto dell’espressione di NPRC/NPRA nel VAT si associa positivamente con colesterolemia (colesterolo totale, LDL e non-HDL), insulinemia e HOMA-INDEX, suggerendo come ad una minore attività degli NP nel tessuto adiposo corrisponda un maggior rischio di insulino resistenza. Dunque, l’induzione dell’NPRC insulino- e glucoso-dipendente negli adipociti potrebbe rappresentare il fattore chiave di collegamento tra sindrome metabolica, ritenzione di sodio e ipertensione arteriosa.The natriuretic peptides (NP) system is involved in the lipid metabolism of adipocytes, through the lipolysis and the thermogenic program. Two receptors mediate the response to NP: the signaling receptor NPRA and the clearance receptor NPRC. Of note, the metabolic effects of NPs largely depend on the expression-ratio of the signaling receptor NPRA to the clearance receptor NPRC. Several studies have shown that the system of lipolytic NP is opposed to the lipogenic insulin. Therefore we examined the insulin-mediated regulation of NP receptors in differentiated human adipocytes obtained from SGBS cells line and in primary visceral human adipocytes, obtained from adipose tissue of patients undergoing nephrectomy. Moreover, we tested the association between NP receptors expression in visceral adipose tissue (VAT) and metabolic profiles in patients undergoing renal surgery. Differentiated human adipocytes from VAT and SGBS cell line were treated with insulin (100 nM) after or not pre-treatment with 100nM wortmannin, a specific PI3K inhibitor of the main insulin signalling pathway that inhibits lipolysis in adipocytes. Further experiments in low-glucose media were also performed to simulate in vivo starving conditions. We observed a potent insulin-mediated and glucose-dependent up-regulation of NPRC through the PI3K pathway in differentiated adipocytes. No effect was observed on NPRA. Protein analysis confirmed that NPRC is increased by insulin and blocked by wortmannin. Low-glucose medium hampered the insulin effect. In the patients, an expression ratio in favor of NPRC in adipose tissue was associated with higher fasting insulinemia, higher HOMA index and higher total, LDL and nonHDL cholesterol. In conclusion, insulin and glucose-dependent NPRC induction in adipocytes, especially in the contest of insulin resistance and increased insulin levels, might be a key factor linking hyperinsulinemia, metabolic syndrome and higher blood pressure.
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Béland, Mireille. "Plasma atrial natriuretic peptide during brief upright and supine exercise in man." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61984.
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Chen, Q. "Role of natriuretic peptides in the response of vascular smooth muscle to injury." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597554.
Full textAbstract:
Vascular smooth muscle cell (VSMC) proliferation with neointima formation is the key feature of restenosis after successful percutaneous transluminal coronary angioplasty (PTCA), which severely limits the clinical benefits of a major option in the treatment of coronary heart disease. To date, the prevention and therapy of restenosis in humans remain limited or unsuccessful. Natriuretic peptides (NP) are powerful inhibitors of VSMC proliferation in vitro. However, the mechanisms by which NP inhibit VSMC proliferation are still nuclear, and neither are the in vivo effects of NP on VSMC proliferation known. This dissertation is addressed to the study of the interaction of the NP system with VSMC under pathological conditions of arterial injury. Normal VSMC from different species or different arteries all expressed NP receptors (NPR), although in different subtypes. Normal rat carotid arteries expressed type-A NPR (NPR-A), whereas normal rabbit ear central arteries expressed exclusively type-B NPR (NPR-B). Despite this difference in normal arteries, neointimal VSMC in both rat and rabbit arteries expressed the same subtype of NPR, type-C (NPR-C) implying the involvement of NPR-C in the regulation of arterial response to injury. In the rabbit model of arterial injury, the media of damaged arteries also expressed NPR-C besides the NPR-B that already exists in normal arteries. Time course experiments of NPR expression in this model showed that NPR-C were upregulated between 5 and 7 days after arterial injury. Affinity cross-linking demonstrated that the molecular weights of reduced NPR-A, NPR-B and NPR-C in arteries were 120, 130 and 64 kDa, respectively. Second messenger assays showed that NPR-A and NPR-B in the normal arteries were coupled with cGMP system, whereas NPR-C was not found to be coupled to the cGMP nor to the cAMP system.
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Addisu, Anteneh. "Natriuretic peptides as a humoral link between the heart and the gastrointestinal system." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002406.
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Addisu, Anteneh. "Natriuretic Peptides As A Humoral Link Between The Heart And The Gastrointetsinal System." Scholar Commons, 2008. https://scholarcommons.usf.edu/etd/110.
Full textAbstract:
Natriuretic peptides are a family of hormones released by several different tissues and exert various physiological functions by coupling with cell surface receptors and increasing intracellular cyclic gyanylyl monophosphate (cGMP). Atrial Natriuretic Peptide (ANP) and B-type Natriuretic Peptide (BNP) are released in response to mechanical stretch of the atrial or ventricular myocardium, respectively and their plasma level is markedly elevated during myocardial infarction and heart failure. Heart failure in turn is associated with symptoms suggestive of perturbed gastrointestinal function such as nausea, indigestion and malabsorption.
Intragastric pressure was monitored using a balloon catheter in anesthetized mice. The pressure before and after treatment with a 10 ng/g intravenous dose of ANP, BNP, CNP or vehicle was compared and analyzed. All the natriuretic peptides significantly decreased intragastric pressure compared to vehicle. These effects were attenuated or absent in natriuretic peptide receptor type-A (NPR-A) knockout mice. Furthermore, the effect of BNP on gastric emptying and intestinal absorption was examined using a meal consisting of fluorescence labeled dextran gavage fed to awake mice. BNP significantly decreased gastric emptying and absorption as compared to vehicle control. Using a cryoinfarction acute myocardial injury model, our investigation showed that mice with acute cryoinfarction had a significantly lower gastric emptying and absorption of a gavage fed meal compared to sham. Circulating BNP levels were significantly higher in the infarcted mice compared to controls. Immunostaining showed amplified distribution of the non-muscle myosin type-II (MCH-II) in BNP treated mice. MCH-II is involved in movement of intestinal villi.
In summary, natriuretic peptides in general and BNP in particular, have gastrointestinal effects including reduced gastric contractility, emptying and absorption. In addition to their effect on smooth muscle relaxation mediated by cGMP, natriuretic peptides appear to have an effect on distribution of MHC-II in cells of the intestinal villi.
We postulate that these effects are aimed at mediating a 'communication' between the cardiovascular and gastrointestinal systems. Further characterization of such a link will not only add a dimension to the understanding of the pathophysiology of heart failure but also enhances the search for further therapeutic targets.
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Hamad, Ahmed El-Sayed Mansour Abd El-Mohsen. "Guanosine 3': 5'-cyclic monophosphate regulation in cultured human airway smooth muscle cells and its role in proliferation." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298959.
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Wu, Shengqian. "Study of atrial natriuretic peptide and endothelin in streptozotocin-diabetic rats and in the aging rats /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19982069.
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McCartney, Shirley. "Atrial natriuretic peptide receptor subtype determination and biological actions of atrial natriuetic peptided in bovine cardiac muscle and hypertensive rat liver." Thesis, University of St Andrews, 1992. http://hdl.handle.net/10023/14455.
Full textAbstract:
Atrial natriuretic peptide (ANP) has previously been shown to bind to specific ANP receptors and increase intracellular cGMP levels in purified rat cardiac sarcolemmal membranes. Experiments described in this thesis were performed to investigate the binding characteristics of ANP in bovine ventricular sarcolemmal membranes and in plasma membranes isolated from the liver of hypertension-resistant and hypertension-sensitive Dahl rats fed on two dietary salt regimes one of 0.8% NaCl and the other 8% NaCl. Additional experiments utilising ANP analogues in radio-receptor assays and radio-receptor crosslinking assays were performed to determine the precise nature of the ANP receptor population present in these membrane preparations. In bovine ventricular cardiac sarcolemmal membranes, ANP bound specifically to one class of ANP receptor with a Kd of approximately 44 pM and a Bmax of approximately 49 fmol/mg protein. ANP produced a 1.8-fold stimulation of manganese-dependent guanylate cyclase activity with an EC50 value of approximately 1 nM. Receptor binding using the des-ANP analogue indicated the predominant presence of the ANP-B receptor subtype. Radioreceptor crosslinking experiments did not entirely agree with these experiments. Radio-receptor crosslinking indicated the presence of two ANP receptors one of 60 kDa and one of 120 kDa, equivalent to the molecular weights of ANP receptors found in other tissues. Collectively these experiments indicate that bovine ventricular sarcolemmal membranes possess ANP receptors, at least a proportion of which are coupled to guanylate cyclase (ANP-B receptors). In plasma membranes from the liver of Dahl-Resistant (Dahl-R) and Dahl-Sensitive (Dahl-S) rats, ANP bound specifically to one class of ANP receptor with Kd values ranging from 245 to 288 pM and Bmax values ranging from 104 to 217 fmol/mg protein. ANP produced a 3.8 to 6.15-fold stimulation of manganese-dependent guanylate cyclase activity with an EC50 values ranging from 2.3 to 7.4 nM, dependent on the strain of Dahl rat and the dietary salt regime used. In liver membranes isolated from rats sensitive to salt-induced hypertension results indicated increases in Bmax with no change in Kd for ANP binding to receptors and higher basal and ANP-stimulated guanylate cyclase levels. Receptor binding using the des-ANP analogue indicated the presence of 13-33% ANP-C receptors with a majority of ANP-B receptors in plasma membranes isolated from the liver of Dahl-R and Dahl-S rats. However, radio-receptor crosslinking experiments were unable to support these results. Collectively these experiments indicate that in plasma membranes isolated from the liver of Dahl-R and Dahl-S rats possess ANP receptors, at least a majority of which are coupled to guanylate cyclase (ANP-B receptors) and that sensitivity to hypertension induced by a high salt dietary regime increases the density of ANP receptors coupled to guanylate cyclase.
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Alehagen, Urban. "Heart failure in primary health care : special emphasis on natriuretic peptides in the elderly /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med819s.pdf.
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Man, Bik-ling, and 文碧玲. "Plasma brain natriuretic peptide and systemic ventricular function after the Fontan procedure." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010365.
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McLeod, Janet Leigh, and janet mcleod@deakin edu au. "The natriuretic peptides and their receptors in the brain of the amphibian, Bufo marinus." Deakin University. School of Biological and Chemical Sciences, 1999. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20071024.112730.
Full textAbstract:
The natriuretic peptides, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are members of a family of hormones that play an important role in mammalian fluid and electrolyte balance. In the periphery, natriuretic peptides reduce blood volume and subsequently blood pressure by increasing renal natriuresis and diuresis and relaxation of vascular smooth muscle. The actions of natriuretic peptides are mediated via two membrane-linked guanylate cyclase receptors (NPR-GC); natriuretic peptide receptor-A (NPR-A) which has a high affinity for ANP and BNP; and natriuretic peptide receptor-B (NPR-B)which has the greatest affinity for CNP. A third receptor not linked to guanylate cyclase, natriuretic peptide receptor-C (NPR-C) also exists, which binds to ANP, BNP and CNP with a relatively equal affinity, and is involved with clearance of the peptides from the circulation and tissues. The natriuretic peptides are present in the brain and are particularly predominant in cardiovascular and fluid and electrolyte regulating areas such as the anteroventral third ventricle (AV3V) region. This distribution has led to the suggestion natriuretic peptides play a neuromodulatory role in the central control of fluid homeostasis. Natriuretic peptides in the brain have been observed to inhibit the release of other fluid and electrolyte regulating hormones such as arginine vasopressin (AVP) and angiotensin II (AII).
Natriuretic peptides have also been identified in the non-mammalian vertebrates although information regarding the distribution of the peptides and their receptors in the non-mammalian brain is limited. In amphibians, immunohistochemical studies have shown that natriuretic peptides are highly concentrated in the preoptic region of the brain, an area believed to be analogous to the A\T3\ region in mammals, which suggests that natriuretic peptides may also be involved in central fluid and electrolyte regulation in amphibians. To date, CNP is the only natriuretic peptide that has been isolated and cloned from the lower vertebrate brain, although studies on the distribution of CNP binding sites in the brain have only been performed in one fish species. Studies on the distribution of ANP binding sites in the lower vertebrate brain are similarly limited and have only been performed in one fish and two amphibian species. Moreover, the nature and distribution of the natriuretic peptide receptors has not been characterised. The current study therefore, used several approaches to investigate the distribution of natriuretic peptides and their receptors in the brain of the amphibian Bufo marinus. The topographical relationship of natriuretic peptides and the fluid and electrolyte regulating hormone arginine vasotocin was also investigated, in order to gain a greater understanding of the role of the natriuretic peptide system in the lower vertebrate brain.
Immunohistochemical studies showed natriuretic peptides were distributed throughout the brain and were highly concentrated in the preoptic region and interpeduncular nucleus. No natriuretic peptide-like immunoreactivity (NP-IR) was observed in the pituitary gland. Arginine vasotocin-like immunoreactivity (AvT-IR) was confined to distinct regions, particularly in the preoptic/hypothalamic region and pituitary gland. Double labelling studies of NP-JR and AvT-IR showed the peptides are not colocalised in the same neural pathways.
The distribution of natriuretic peptide binding sites using the ligands 125I-rat ANP (125I-rANP) and 125I-porcine CNP (125I-pCNP) showed different distributions in the brain of B. marinus. The specificity of binding was determined by displacement with unlabelled rat ANP, porcine CNP and C-ANF, an NPR-C specific ligand. 125I-rANP binding sites were broadly distributed throughout the brain with the highest concentration in pituitary gland, habenular, medial pallium and olfactory region. Minimal 125I-rANP binding was observed in the preoptic region. Residual 125I-rANP binding in the presence of C-ANF was observed in the olfactory region, habenular and pituitary gland indicating the presence of both NPR-GC and NPR-C in these regions. 125I-pCNP binding was limited to the olfactory region, pallium and posterior pituitary gland. All 125I-pCNP binding was displaced by C-ANF which suggests that CNP in the brain of B. marinus binds only to NPR-C.
Affinity cross-linking and SDS-PAGB demonstrated two binding sites at 136 kDa and 65 kDa under reducing conditions. Guanylate cyclase assays showed 0.1 µM ANP increased cGMP levels 50% above basal whilst a 10-fold higher concentration of CNP was required to produce the same result. Molecular cloning studies revealed a 669 base pair fragment showing 91% homology with human and rat NPR-A and 89% homology with human, rat and eel NPR-B. A 432 base pair fragment showing 67% homology to the mammalian NPR-C and 58% homology with eel NPR-D was also obtained.
The results show natriuretic peptides and their receptors are distributed throughout the brain of B. marinus which indicates that natriuretic peptides may participate in a range of regulatory functions throughout the brain. The potential for natriuretic peptides to regulate the release of the fluid and electrolyte regulating hormone AVT also exists due to the high number of natriuretic peptide binding sites in the posterior pituitary gland. At least two populations of natriuretic peptide receptors are present in the brain of B. marinus, one linked to guanylate cyclase and one resembling the mammalian clearance receptor. Furthermore, autoradiography and guanylate cyclase studies suggest ANP may be the major ligand in the brain of B. marinus, even though CNP is the only natriuretic peptide that has been isolated from the lower vertebrate brain to date.
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Panayiotou, C. M. "Characterisation of the anti-inflammatory and anti-proliferative effects of natriuretic peptides in rodents." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445064/.
Full textAbstract:
Natriuretic peptides are a family of vasoactive hormones that play important roles in cardiovascular homeostasis. These peptides exert biological effects primarily via activation of guanylate cyclase (GC)-coupled natriuretic peptide receptors (NPR) that generate the intracellular messenger cyclic guanosine 3',5'-monophosphate (cGMP). Activation of the cytosolic GC by NO is well-established to mediate cGMP-dependent, anti-atherogenic effects however, an analogous cytoprotective role for natriuretic peptides has yet to be fully elucidated. Since many cardiovascular disorders (e.g. atherosclerosis, septic shock) are now accepted as inflammation-based diseases, identification of potential roles for natriuretic peptides in regulating vascular inflammation might assist in the prevention and treatment of cardiovascular pathology. The studies described in this thesis investigated the hypothesis that natriuretic peptides (i.e. atrial natriuretic peptide ANP , C-type natriuretic peptide CNP ) affect pro-inflammatory protein expression (i.e. inducible NO synthase, iNOS) and cell proliferation via activation of GC-linked NPR. Herein, it is demonstrated that in NPR-A knockout mice, iNOS expression and NO production in response to intravenous administration of bacterial lipopolysaccharide is significantly reduced compared to wild-type controls this difference is mirrored in the ex vivo functional reactivity of vessels from such animals. However, neither ANP nor CNP were able to alter iNOS expression or NO production in vitro in RAW264.7 murine macrophages or primary rat aortic smooth muscle cells. CNP, but not ANP, transiently enhanced phosphorylation of extracellular signal-regulated kinase (ERK)1/2. CNP-induced ERK 1/2 phosphorylation was blocked by the selective ERK 1/2 inhibitor PD98059, the Gj-protein inhibitor Pertussis toxin, and the selective NPR-C antagonist M372049. Accordingly, CNP inhibited vascular smooth muscle proliferation in a PD98059- and M372049-reversible manner. These observations suggest that part of the anti-atherogenic profile of CNP is mediated via NPR-C, Gi-dependent ERK 1/2 phosphorylation and inhibition of vascular smooth muscle proliferation. Moreover, my findings identify a potential pro-inflammatory role for ANP/NPR-A-dependent signalling in vivo.
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Chun, Taehwa. "Regulation of expression of endothelium-derived relaxing peptides, C-type natriuretic peptide and adrenomedullin by shear stress and oxidative stress." Kyoto University, 2001. http://hdl.handle.net/2433/150548.
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Marttila, M. (Minna). "Paracrine and transcription factors mediating the natriuretic peptide gene expression during hemodynamic stress." Doctoral thesis, Oulun yliopisto, 1999. http://urn.fi/urn:isbn:951425449X.
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Abstract
Cardiac pathologies, including ventricular hypertrophy, are the primary cause of death in industrialized countries. Cardiac hypertrophy is often the consequence of work overload on the heart and characterizes several cardiovascular diseases, including atherosclerosis and hypertension. Cardiac hypertrophy is accompanied by genetic reprogramming characterized by the reexpression of several embryonic and growth response genes. Two of these genes encode A- and B-type natriuretic peptides (ANP and BNP), two cardiac-specific hormones secreted by myocytes, which play an important role in blood pressure regulation. The aim of the present study was to study the effect of acute pressure overload on BNP gene expression in the hearts of normal and hypertensive rats and then to examine the role of a passerine factor, angiotensin II (Ang II), on volume and pressure overload -induced ANP and BNP secretion and synthesis. Further, the aim was to characterize elements on the BNP promoter mediating hemodynamic stress in vivo.
BNP gene expression was studied in conscious spontaneously hypertensive (SHR) rats and together with ANP in two hypertensive, ream Transgenic rat models. The increased workload of the heart was produced by the infusion of vasopressin (AVP), phenylephrine (PHE) or bolus saline infusion. The increased workload caused rapid increases in cardiac BNP mRNA levels. Daring both AVP and PHE infusions, substantial increases in ventricular BNP mRNA levels were already evident after I h, and peak levels of BNP mRNA were reached at 4 h. Transgenic rats carrying one extra mouse renin gene showed impaired secretion and synthesis of ANP and BNP, while double transgenic rats carrying both human angiotensinogen and human renin genes showed augmentation of left atrial, but not ventricular BNP gene expression in response ta acute pressure overload. To characterize the elements mediating hemodynamic stress, bi-lateral nephrectomy was performed. GATA motif transduced the hemodynamic stress stimulus 26–28 hrs postnephrectomy in BNP gene expression.In conclusion, these results show that pressure overload abruptly stimulates the cardiac expression of a noncontractile protein gene BNP, suggesting that it may be used as a myocyte-specific marker of mechanical loading. BNP gene expression was augmented in atria hut nut in ventricles in response to pressure overload in an experimental model of hypertension, suggesting that high local levels of Ang II may differentially regulate cardiac gene expression in atrial and ventricular myocytes in double transgenic rats. At the transcriptional level, acute hemodynamic stress produced by nephrectomy increases BNP reporter expression through a GATA-dependent pathway.
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Kinnunen, P. (Pietari). "Adrenomedullin as a regulator of cardiac function." Doctoral thesis, University of Oulu, 2000. http://urn.fi/urn:isbn:9514256751.
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Abstract
Adrenomedullin (AM) is a 52-amino acid peptide which is produced
in many tissues, including adrenal medulla, lung, kidney and heart.
Intravenous administration of AM causes a long-lasting hypotensive
effect, accompanied with an increase in the cardiac output in experimental
animals. This study was aimed to examine whether AM has any direct
effects on myocardial function. In addition to the myocardial contractility,
the effects of AM on coronary vascular tone and A-type natriuretic
peptide (ANP) release from atria and B-type natriuretic peptide
(BNP) gene expression in the ventricles were studied in the perfused
rat heart preparation.
In spontaneously beating hearts, AM had no effects on the
heart rate, but dose-dependently increased the developed tension
(DT) with an EC50 of 7 x 10-11 nmol/l,
reflecting a potent positive inotropic effect. The lower the initial
resting tension, the higher was the elevation in DT. In paced hearts,
a protein kinase A inhibitor, H-89, had no effect on AM-induced
inotropic effect, and AM did not increase the cAMP content of the
ventricular myocardium. In contrast, the inhibitors of sarcoplasmic
reticulum Ca2+ stores, ryanodine
and thapsigargin, as well as a protein kinase C inhibitor, staurosporine,
significantly attenuated the inotropic response to AM. L-type Ca2+ channel blocker,
diltiazem, also suppressed the AM-induced elevation in DT. Moreover,
AM increased the duration of myocyte action potentials between 10
mV and - 50 mV in isolated rat atria, consistent with an
increase in L-type Ca2+ channel
current during the plateau.
Inotropic effect of endothelin-1 (ET-1), another locally
acting peptide, was enhanced by inhibiting the myocardial nitric
oxide (NO) synthesis by Nω-nitro-L-arginine
methyl ester (L-NAME) in perfused rat heart. The AM-induced inotropic
action was unaltered by L-NAME treatment. When AM and ET-1 were
administrated in combined infusion, the inotropic response was significantly smaller
than that following the infusion of the peptides alone. This attenuated
response was more than overcome by infusion of L-NAME, although
the individual responses to AM and ET-1 were not modulated by L-NAME
at the doses used in the combination. Consistent with its vasodilator
action, AM dose-dependently dilated the coronary arteries of the
perfused heart. The effect of AM was not dependent on NO under basal
conditions or in coronary arteries constricted with ET-1. Furthermore, AM
enhanced the stretch-induced release of ANP from the right atrium,
but did not affect the ventricular BNP expression induced by ET-1.
In conclusion, AM exerts regulatory actions on the heart
by increasing cardiac contractility, dilating coronary arteries
and modulating stretch-induced ANP release. The inotropic effect
of AM was independent of cyclic AMP, but may involve activation
of protein kinase C, Ca2+ influx
through L-type Ca2+ channels
and the release of Ca2+ from
the sarcoplasmic reticulum. Endogenous NO production did not modulate
the inotropic effect of AM, although the effect of ET-1 was suppressed. Combined
administration of AM and ET-1 produced a weak inotropic response
most likely because of a potentiated synthesis of NO. Finally, AM
had a coronary vasodilator effect and augmented the stretch-induced
ANP release in the right atrium.
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Suo, M. (Maria). "The role and mechanisms of angiotensin II in regulating the natriuretic peptide gene expression in response to cardiac overload." Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514266994.
Full textAbstract:
Abstract
Heart responds to pathological hemodynamic stress by increasing cardiac myocyte size, reprogramming gene expression and enhancing contractile protein synthesis. Neurohumoral factors mediate hypertrophic adaptation either directly via specific receptors or indirectly by increasing blood pressure and cardiac load. The aim of this study was to evaluate the role of angiotensin II (Ang II) in the atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) gene expression during cardiac overload. Furthermore, the mechanisms of action of Ang II in regulating cardiac gene expression were studied.
Hemodynamic stress was produced by Ang II or nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) administration in conscious rats. Despite hypertension and increased left ventricular ANP and BNP mRNA levels, L-NAME administration for 8 weeks did not induce left ventricular hypertrophy. Ang II type 1 receptor (AT1) antagonism decreased significantly L-NAME-induced hypertension and ventricular ANP gene expression. Ang II-induced cardiac overload produced significant increase in ventricular ANP and BNP mRNA levels at 12 and 72 h, respectively. To study whether the factors synthesized by adrenals modulate the response of Ang II, the effects of adrenalectomy were studied. In Ang II-treated rats, adrenalectomy either abolished or blunted the early activation of ANP and BNP gene expression, respectively.
Ang II infusion for 2 weeks increased cardiac mass and blood pressure measured by telemetry, and produced changes in diastolic function detected by echocardiography. By using direct plasmid DNA injections into the rat myocardium, BNP promoter activity was observed to increase at 2 h and remain up-regulated up to 2 weeks of Ang II infusion, except at 12 h. BNP mRNA levels increased at 2 h but decreased to basal levels after 72 h. Mutation of GATA elements of the BNP promoter and DNA binding assays revealed that GATA4 mediates the Ang II-responsiveness of the BNP gene.
These results indicate that Ang II plays an important role in regulating
natriuretic peptide gene expression during cardiac overload. ANP and BNP gene
expression in the rat heart is modulated by the adrenal factors during Ang II-stimulated hemodynamic stress and the AT1 receptor antagonism in NO-deficient hypertension. Moreover, ventricular BNP gene expression in Ang II-induced hypertension in vivo is controlled by posttranscriptional mechanisms and GATA elements.
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Mäkikallio, A. (Anne). "Cardiovascular autonomic and hormonal dysregulation in ischemic stroke with an emphasis on survival." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514278526.
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Abstract
Ischemic stroke is associated with cardiovascular autonomic nervous system (ANS) disturbances, including reduced heart rate (HR) variability and acute phase neurohumoral activation with elevated stress hormone levels. The impact of HR variability and neurohumoral factors such as natriuretic peptides on the long-term survival of patients with ischemic stroke has not been studied previously. This study was designed to evaluate cardiovascular autonomic regulation in ischemic stroke patients by assessing HR dynamics and various neurohumoral factors. The values of the assessed variables in predicting mortality were evaluated.
HR variability assessments were performed in the acute phase of ischemic stroke and for a general elderly population. Various neurohumoral factors were also assessed in the acute phase of stroke. After follow-up, the survival of the subjects was assessed and the prognostic values of the measured factors were evaluated.
Stroke patients were found to have cardiovascular autonomic and hormonal disturbances manifested as reduced traditional time and frequency domain measures of HR variability, altered long-term HR dynamics and elevated levels of natriuretic peptides in the acute phase. Altered long-term HR dynamics in the acute phase of stroke predicted long-term mortality after stroke and cerebrovascular mortality in the general elderly population. Neuroendocrine activation involving elevated natriuretic peptide values that were associated with high cortisol and catecholamine levels was observed in the acute phase of ischemic stroke. Neurohumoral disturbance was prognostically unfavourable. The most powerful predictors of poststroke mortality were altered long-term HR dynamics and elevated levels of natriuretic peptides and cortisol, which predicted mortality independently of the conventional risk factors in multivariate analysis.
Prognostically unfavourable cardiovascular autonomic dysfunction with disturbances in the long-term behaviour of HR dynamics was found to be related to ischemic stroke. Neurohormonal activation with elevated natriuretic peptide and cortisol levels in the acute phase predicts long-term mortality after ischemic stroke.
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Luodonpää, M. (Marja). "Adrenomedullin and natriuretic peptides in cardiac hypertrophy:regulation of gene expression and interactions with angiotensin II." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514275578.
Full textAbstract:
Abstract
The heart responds to increased hemodynamic stress by increased cardiac myocyte size, enhanced protein synthesis and altered gene expression. Regulation of hypertrophic adaptation involves a number of neural and hormonal factors, which act on the cardiovascular system. The aim of the present study was to elucidate the regulation of gene expression of natriuretic peptides and adrenomedullin (AM) in cardiac overload in vivo. Furthermore, the interactions of AM and angiotensin II (Ang II) in cardiac function and development of left ventricular hypertrophy were studied both in vivo and in vitro.
The effects of cardiac hypertrophy on the regulation of natriuretic peptides (atrial natriuretic peptide, ANP and B-type natriuretic peptide, BNP) and AM gene expression were studied during pressure overload in the hearts of two hypertensive rat strains, angiotensinogen-renin transgenic rats and spontaneously hypertensive rats as well as their normotensive control strains. Increased workload resulted in rapid upregulation of both BNP and AM gene expression in all rat strains; the response of AM was, however, augmented in hypertensive rats. Direct left ventricular wall stretch induced AM gene expression in isolated, perfused rat hearts, whereas stretching of cultured cardiac myocytes downregulated AM mRNA levels.
In cultured cardiac cells exposed to Ang II, endothelin-1 or the α-agonist phenylephrine, Ang II-induced myocyte hypertrophy was selectively inhibited by AM. In vivo, AM interacted with Ang II in circulation by attenuating the hypertensive effects of Ang II, and in the heart by augmenting the Ang II-induced improvement in cardiac systolic function. However, AM had no direct modulatory effects on Ang II-induced left ventricular hypertrophy.
These results show that cardiac wall stretch is a major stimulus for the early induction of AM gene expression in both normal and hypertrophied ventricle, and the response in hypertrophied myocardium is augmented. Furthermore, cardiac non-muscle cells may be involved in mediating effects of direct stretch. In vitro, AM acts as a selective inhibitor of Ang II-induced myocyte hypertrophy, suggesting a cardioprotective role for AM to counteract the local renin-angiotensin system and Ang II in cardiac hypertrophy and heart failure. Circulating AM appears to act mainly as a regulator of vascular tone and cardiac function.
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Singer, Donald Robert James. "Studies of the importance of atrial natriuretic peptides in physiology, pathophysiology and treatment in man." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262349.
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In this thesis an attempt has been made to try to dissect out the relative importance of atrial natriuretic peptides (ANP) and the renin-angiotensin-aldosterone system in the control of sodium balance in normal man. At the same time the thesis examines the relevance of ANP in the pathophysiology of essential hypertension and cardiac transplantation and the potential therapeutic value of manipulating the ANP system. The studies described in this thesis were important in suggesting a dominant role of suppression of the renin-angiotensin-aldosterone system in permitting excretion of short term increases in intravenous or oral sodium intake. The permissive effects of suppression of angiotensin II or aldosterone for the excretion of an intravenous sodium load showed clear time differences, with suppression of angiotensin II important immediately but the response to suppression of aldosterone delayed. In contrast, there appears to be only a transient role for changes in circulating levels of ANP in the response to an intravenous sodium load and little evidence that changes in ANP release are important in responding to acute increases in dietary sodium intake in normal subjects. However, the sensing mechanism for ANP release is clearly activated by sustained changes in dietary sodium intake. Studies of prolonged dietary sodium alteration in normal subjects clear evidence for a role of ANP in the medium term regulation of sodium balance and further dietary studies suggested an important role for the ANP system in pathophysiology in essential hypertension and in cardiac transplant recipients.
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Loke, Ian. "Screening for left ventricular dysfunction in the general population using natriuretic peptides and the electrocardiogram." Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29535.
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One thousand three hundred and sixty subjects without a prior diagnosis of heart failure of left ventricular systolic dysfunction were randomly selected from a general population in Leicestershire. All subjects had a transthoracic echocardiogram performed as well as a standard 12 lead electrocardiogram (ECG). Serum levels of N-ANP, BNP and N-BNP were analyzed. There were twenty-eight cases (2.1% of the population) of left ventricular systolic dysfunction (LVSD), defined as a wall motion score index of >1.8. Serum levels of all three cardiac peptides were significantly elevated in subjects with LVSD. The prevalence of electrocardiographic abnormalities was also higher in the LVSD population. Using multivariate logistic regression analysis, ECG abnormalities, including a prolonged QRS duration, as well as N-ANP, BNP and N-BNP independently predicted LVSD. I then analyzed the performance of cardiac peptides and the ECG in diagnosing LVSD. All three cardiac peptides had high negative predictive values but low positive predictive values. The ECG performed less well as compared to cardiac peptides in diagnosing LVSD. BNP consistently performed better than N-ANP and N-BNP. Combining the ECG to any of the three cardiac peptides improved the diagnostic utility for LVSD.
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Ala-Kopsala, M. (Minna). "Circulating N-terminal fragments of A- and B-type natriuretic peptides: molecular heterogeneity, measurement and clinical application." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514282469.
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Natriuretic peptides have emerged as important candidates for the development of diagnostic tools in cardiovascular disease. Their increased concentrations have been found to be useful for ruling out disease of cardiac origin, as prognostic indicators, and in the follow-up of patients with heart failure. In order for natriuretic peptides to be efficient biomarkers, analytical problems in assay specificity and calibration need to be resolved. The aim of the present study was to elucidate circulating molecular components of N-terminal fragments of A- and B-type natriuretic peptides (NT-proANP and NT-proBNP) in human blood, and to develop reliable and novel assays for their measurement with clinical application.
Reliable immunoassays for NT-proANP and NT-proBNP were set up based on recombinant calibrators and antisera against different epitopes. A novel immunoassay for detecting the activation of A- and/or B-type natriuretic peptide systems, referred to as NT-proXNP, was also developed. The chromatographic results of human plasma and serum samples indicated that NT-proANP and especially NT-proBNP are heterogeneous in human circulation. They are truncated at both termini, causing a serious risk of preanalytical errors. Further studies with recombinant peptides confirmed that the central parts of NT-proANP and NT-proBNP are stable in plasma and serum even at harsh storage conditions. Thus the most reliable assays are directed at the central portions of the molecule only.
All developed assays were applicable to clinical samples of cardiac patients. NT-proXNP showed a diagnostic efficiency equal to or slightly better compared to individual NT-proANP and NT-proBNP assays. Furthermore, the prognostic value of NT-proANP and NT-proBNP was investigated in a population-based sample of men. Both peptides were strong predictors of mortality and its co-morbidities, adding to the prognostic value of conventional risk factors.
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Grieg, Bryan. "A biochemical and pharmacological analysis of novel natriuretic peptides from the venoms of Australian elapid snakes /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16091.pdf.
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Doust, Jenny. "Managing uncertainty in diagnostic decision making : B-type natriuretic peptide for the diagnosis and management of heart failure /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19791.pdf.
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Vierimaa, H. (Heidi). "Salmon cardiac peptide as a model for natriuretic peptide secretion:the role of mechanical load, temperature and endothelin-1." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514282000.
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Abstract
The natriuretic peptides are a family of hormones secreted by the heart. They play a fundamental role in salt and water balance and blood pressure regulation. Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are the known members of the mammalian natriuretic peptide family. A major stimulus for the secretion of cardiac natriuretic peptides is myocyte stretch. Therefore, the secretion of natriuretic peptides is increased in response to elevated blood volume. Natriuretic peptide production and release is also affected by several other factors, such as endothelin-1 (ET-1), acting in paracrine fashion.
The aim of this study was to elucidate factors regulating the novel cardiac peptide hormone, salmon cardiac peptide (sCP), belonging to the family of natriuretic peptides. The role of mechanical load, temperature and ET-1 in sCP secretion and production was studied using in vitro (isolated perfused ventricle preparation) and in vivo methods. Comparisons between the natriuretic peptide systems in fish and mammals were done to clarify functional evolution of this hormone family. Salmon (Salmo salar) was selected as a model, since it has an outstanding adaptability to wide variations in environmental salinity and has developed defence mechanisms against volume or salt load.
The results showed that salmon ventricle stores large amounts of the prohormone of sCP, whereas the secreted form is the mature 29-amino acid form. The N-terminal fragment of pro-sCP is co-secreted with sCP in equimolar amounts. sCP is released rapidly in response to appropriate stimulus, whereas induction of its gene expression is slower. Mechanical load is an important regulator of sCP secretion. Temperature also plays a major role in regulating sCP plasma concentration by affecting its elimination from circulation. Additionally, ET-1 is a potent secretagogue of the sCP system and an inotropic agent in salmon heart. Furthermore, the present results reveal remarkable synergism between the cardiac effects of ET-1 and β-adrenergic stimulation.
In conclusion, the sCP system in salmon ventricle largely resembles the ANP system in mammalian atrium, while also having specific characteristics, such as a regulated ventricular natriuretic peptide secretion pathway. Therefore, the sCP system offers a unique model for studying mechanisms of natriuretic peptide biology.
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Macaulay, Hunter Esther Frances. "The measurement of Pro Atrial Natriuretic Peptide and derived peptides, in health and heart disease, using several 'two-site' immunoradiometric assays and radioimmunoassays." Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357706.
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Yasuno, Shinji. "Endogenous cardiac natriuretic peptides protect the heart in a mouse model of dilated cardiomyopathy and sudden death." Kyoto University, 2010. http://hdl.handle.net/2433/97945.
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