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Academic literature on the topic 'Natriuretic peptides'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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Journal articles on the topic "Natriuretic peptides"

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Kovács, L. Gábor, Noémi Nyolczas, Tamás Habon, Róbert Sepp, Zsolt Piroth, Ágota Hajas, Imre Boncz, János Tomcsányi, János Kappelmayer, and Béla Merkely. "Natriureticus peptidek mérése szívelégtelen betegekben: a helyes laboratóriumi és klinikai gyakorlat." Orvosi Hetilap 156, no. 31 (August 2015): 1235–45. http://dx.doi.org/10.1556/650.2015.30219.

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Cardiac natriuretic peptides (BNP, NT-proBNP) play a pivotal role in cardiovascular homeostasis, mainly due to their roles in vasodilatation, natriuresis, diuresis and due to their antiproliferative properties. Proper measurement of the natriuretic peptide levels may help differentiate between respiratory and cardiac forms of dyspnea, diagnose early forms of heart failure, evaluate severity of heart failure (prognosis) and monitor the efficacy of therapy. In many countries natriuretic peptide levels are being used as one of the earliest diagnostics tools to evaluate the involvement of the heart. Current theoretical and clinical data confirm the importance of natriuretic peptides in routine healthcare. These roles are clearly described in international recommendations and guidelines. In the current review the authors discuss the problems of the measurement of natriuretic peptides in Hungary, including several aspects related to laboratory medicine, cardiology and health economy. Orv. Hetil., 2015, 156(31), 1235–1245.

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Lee, Noel S., and Lori B. Daniels. "Current Understanding Of The Compensatory Actions Of Cardiac Natriuretic Peptides in Cardiac Failure: A Clinical Perspective." Cardiac Failure Review 2, no. 1 (2016): 14. http://dx.doi.org/10.15420/cfr.2016:4:2.

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Natriuretic peptides play a crucial role in maintaining cardiovascular homeostasis. Among their properties are vasodilation, natriuresis, diuresis, and inhibition of cardiac remodeling. As heart failure progresses, however, natriuretic peptides fail to compensate. Knowledge of their processing and signaling pathways has guided the development of pharmacological therapies aimed at bolstering their effects. The drugs that have achieved the most clinical success have also stirred the most controversy. Nesiritide, the synthetic B-type natriuretic peptide, yielded significant symptomatic relief and improved haemodynamics but its use was plagued with questions surrounding its possibly harmful impact on renal function. More recently, compounds containing inhibitors of neprilysin, the enzyme responsible for degrading natriuretic peptides, have demonstrated morbidity and mortality benefit, but have also been linked to possible negative side effects. Clearly, potentiating the actions of natriuretic peptides for the benefit of patients is not as simple as just raising their serum concentration. This article reviews the current understanding of the compensatory actions of cardiac natriuretic peptides in heart failure and how this knowledge is revolutionizing heart failure therapy.

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BORGESON, Daniel D., Tracy L. STEVENS, Denise M. HEUBLEIN, Yuzuru MATSUDA, and John C. BURNETT. "Activation of myocardial and renal natriuretic peptides during acute intravascular volume overload in dogs: functional cardiorenal responses to receptor antagonism." Clinical Science 95, no. 2 (August 1, 1998): 195–202. http://dx.doi.org/10.1042/cs0950195.

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1.A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2.Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10% of body weight over 1 ;h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0±4.2 versus 62±8.0 ;pg/min, P< 0.05). 3.In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6±1.1 to 5.0±1.2 ;pmol/ml, P< 0.05). A significant attenuation of natriuresis (566±91 versus 1241±198 ;μEq/min, P< 0.05) and diuresis (4.8±0.7 versus 10.1±2.0 ;ml/min, P< 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4.These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.

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Song, H., J. Papadimitriou, C. Drachenberg, M. R. Weir, and C. Wei. "Enhancement of Natriuretic Peptides in Rejected Human Renal Graft." Microscopy and Microanalysis 6, S2 (August 2000): 602–3. http://dx.doi.org/10.1017/s1431927600035509.

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Natriuretic peptides include atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). ANP, BNP and CNP are structure related but genetic distinct 1 natriuretic peptide family. ANP and BNP are cardiac cell origin and CNP are endothelial cell and kidney origin. Natriuretic peptides have potent vasoactive and natriuretic actions through generation of cGMP. On the other hand, renal graft rejection is major problem after kidney transplantation with severe renal damage and renal vasoconstriction. We hypothesized that renal tissue level of natriuretic peptides increase in renal graft rejection through compensatory mechanism. Therefore, the present study was designed to determine the expression of natriuretic peptides by immunohistochemical staining (IHCS) in human renal tissue with rejection and compare with normal renal tissue.Human renal biopsy (n=5) were obtained after kidney transplantation with mild and moderate renal rejection. Normal kidney biopsy was obtained during nephrectomy. ANP, BNP and CNP levels in renal tissue were determined by IHCS.

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Hagiwara, H., A. Inoue, A. Yamaguchi, S. Yokose, M. Furuya, S. Tanaka, and S. Hirose. "cGMP produced in response to ANP and CNP regulates proliferation and differentiation of osteoblastic cells." American Journal of Physiology-Cell Physiology 270, no. 5 (May 1, 1996): C1311—C1318. http://dx.doi.org/10.1152/ajpcell.1996.270.5.c1311.

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The effects of natriuretic peptides on the proliferation and differentiation of osteoblast-like cells from rat calvariae were examined. Natriuretic peptides are physiological agonists that activate receptor guanylate cyclases, namely, natriuretic peptide receptor (NPR)-A and NPR-B. Exposure of cells to atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) resulted in large increases in the rate of intracellular production of guanosine 3',5'-cyclic monophosphate (cGMP). Moreover, CNP-like immunoreactivity was detected in the conditioned medium from osteoblast-like cells, while ANP was undetectable. In cells exposed to natriuretic peptides, a dose-dependent reduction in the rate of DNA synthesis was observed. Natriuretic peptides also stimulated the activity of alkaline phosphatase (ALPase) and the expression of mRNA for ALPase and osteocalcin and the mineralization of nodules by the cultured cells. These results could be reproduced by treating cells with 8-bromo-cGMP. Endothelin-1, whose physiological functions are the opposite of those of natriuretic peptides, decreased the ALPase activity and the mineralization of nodules. In the present study, natriuretic peptides were demonstrated to promote bone formation via the action of cGMP in a signal-transduction pathway mediated by specific receptors in osteoblast-like cells.

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Arjamaa, Olli, and Mikko Nikinmaa. "Natriuretic peptides in hormonal regulation of hypoxia responses." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 2 (February 2009): R257—R264. http://dx.doi.org/10.1152/ajpregu.90696.2008.

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The possibility that natriuretic peptides' effects are important in hypoxia responses of vertebrates is reviewed. Both the transcription and release of natriuretic peptides are affected by oxygen tension. Furthermore, many of the effects observed in hypoxia, such as diuresis and a reduction of plasma volume, are also caused by treatment of the animal with natriuretic peptides. Also, several clinical observations about changes in natriuretic peptide levels in, e.g., sleep apnea and cyanotic congenital heart disease, are consistent with the idea that hypoxia is involved in the etiology of conditions, in which natriuretic peptide levels increase. Virtually all published information on the relationship between oxygen and natriuretic peptides is based on human studies. Because hypoxic conditions are more common in aquatic than terrestrial environments, future studies about the possible role of natriuretic peptides in hypoxia, as well as the role of hypoxia in the evolution of natriuretic peptides, including the different subtypes, should increasingly involve also aquatic organisms.

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Geelhoed, Bastiaan, Christin S. Börschel, Teemu Niiranen, Tarja Palosaari, Aki S. Havulinna, Césaire J. K. Fouodo, Markus O. Scheinhardt, et al. "Assessment of causality of natriuretic peptides and atrial fibrillation and heart failure: a Mendelian randomization study in the FINRISK cohort." EP Europace 22, no. 10 (August 23, 2020): 1463–69. http://dx.doi.org/10.1093/europace/euaa158.

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Abstract Aims Natriuretic peptides are extensively studied biomarkers for atrial fibrillation (AF) and heart failure (HF). Their role in the pathogenesis of both diseases is not entirely understood and previous studies several single-nucleotide polymorphisms (SNPs) at the NPPA-NPPB locus associated with natriuretic peptides have been identified. We investigated the causal relationship between natriuretic peptides and AF as well as HF using a Mendelian randomization approach. Methods and results N-terminal pro B-type natriuretic peptide (NT-proBNP) (N = 6669), B-type natriuretic peptide (BNP) (N = 6674), and mid-regional pro atrial natriuretic peptide (MR-proANP) (N = 6813) were measured in the FINRISK 1997 cohort. N = 30 common SNPs related to NT-proBNP, BNP, and MR-proANP were selected from studies. We performed six Mendelian randomizations for all three natriuretic peptide biomarkers and for both outcomes, AF and HF, separately. Polygenic risk scores (PRSs) based on multiple SNPs were used as genetic instrumental variable in Mendelian randomizations. Polygenic risk scores were significantly associated with the three natriuretic peptides. Polygenic risk scores were not significantly associated with incident AF nor HF. Most cardiovascular risk factors showed significant confounding percentages, but no association with PRS. A causal relation except for small causal betas is unlikely. Conclusion In our Mendelian randomization approach, we confirmed an association between common genetic variation at the NPPA-NPPB locus and natriuretic peptides. A strong causal relationship between natriuretic peptides and incidence of AF as well as HF at the community-level was ruled out. Therapeutic approaches targeting natriuretic peptides will therefore very likely work through indirect mechanisms.

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Levin, E. R. "Natriuretic peptide C-receptor: more than a clearance receptor." American Journal of Physiology-Endocrinology and Metabolism 264, no. 4 (April 1, 1993): E483—E489. http://dx.doi.org/10.1152/ajpendo.1993.264.4.e483.

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The natriuretic peptide family of proteins acts through two distinct classes of receptors that signal through entirely different mechanisms. The elucidation of the structure of the guanylate cyclase-containing receptor proteins has provided a better understanding of the mechanisms by which the natriuretic peptides regulate diverse functions of salt and water balance, in conjunction with other vasoactive peptides. A second receptor class was named for the originally described function of this protein to clear the natriuretic peptides from plasma. The mechanism of signaling for the natriuretic peptide clearance receptor is not firmly established. All known members of the natriuretic peptide family bind to, and can theoretically act through, the clearance receptor. This review summarizes the known features of the natriuretic peptide clearance receptor, a protein that contains extracellular and transmembrane domains and a short cytoplasmic segment. Recent studies have pointed to new and potentially important functions for this protein in mediating the actions of the natriuretic peptides.

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Nakagawa, Hitoshi, and Yoshihiko Saito. "Roles of Natriuretic Peptides and the Significance of Neprilysin in Cardiovascular Diseases." Biology 11, no. 7 (July 6, 2022): 1017. http://dx.doi.org/10.3390/biology11071017.

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Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) activate the guanylyl cyclase A receptor (GC-A), which synthesizes the second messenger cGMP in a wide variety of tissues and cells. C-type natriuretic peptide (CNP) activates the cGMP-producing guanylyl cyclase B receptor (GC-B) in chondrocytes, endothelial cells, and possibly smooth muscle cells, cardiomyocytes, and cardiac fibroblasts. The development of genetically modified mice has helped elucidate the physiological roles of natriuretic peptides via GC-A or GC-B. These include the hormonal effects of ANP/BNP in the vasculature, autocrine effects of ANP/BNP in cardiomyocytes, and paracrine effects of CNP in the vasculature and cardiomyocytes. Neprilysin (NEP) is a transmembrane neutral endopeptidase that degrades the three natriuretic peptides. Recently, mice overexpressing NEP, specifically in cardiomyocytes, revealed that local cardiac NEP plays a vital role in regulating natriuretic peptides in the heart tissue. Since NEP inhibition is a clinically accepted approach for heart failure treatment, the physiological roles of natriuretic peptides have regained attention. This article focuses on the physiological roles of natriuretic peptides elucidated in mice with GC-A or GC-B deletion, the significance of NEP in natriuretic peptide metabolism, and the long-term effects of angiotensin receptor-neprilysin inhibitor (ARNI) on cardiovascular diseases.

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Potter, Lincoln R., Sarah Abbey-Hosch, and Deborah M. Dickey. "Natriuretic Peptides, Their Receptors, and Cyclic Guanosine Monophosphate-Dependent Signaling Functions." Endocrine Reviews 27, no. 1 (November 16, 2005): 47–72. http://dx.doi.org/10.1210/er.2005-0014.

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Natriuretic peptides are a family of structurally related but genetically distinct hormones/paracrine factors that regulate blood volume, blood pressure, ventricular hypertrophy, pulmonary hypertension, fat metabolism, and long bone growth. The mammalian members are atrial natriuretic peptide, B-type natriuretic peptide, C-type natriuretic peptide, and possibly osteocrin/musclin. Three single membrane-spanning natriuretic peptide receptors (NPRs) have been identified. Two, NPR-A/GC-A/NPR1 and NPR-B/GC-B/NPR2, are transmembrane guanylyl cyclases, enzymes that catalyze the synthesis of cGMP. One, NPR-C/NPR3, lacks intrinsic enzymatic activity and controls the local concentrations of natriuretic peptides through constitutive receptor-mediated internalization and degradation. Single allele-inactivating mutations in the promoter of human NPR-A are associated with hypertension and heart failure, whereas homozygous inactivating mutations in human NPR-B cause a form of short-limbed dwarfism known as acromesomelic dysplasia type Maroteaux. The physiological effects of natriuretic peptides are elicited through three classes of cGMP binding proteins: cGMP-dependent protein kinases, cGMP-regulated phosphodiesterases, and cyclic nucleotide-gated ion channels. In this comprehensive review, the structure, function, regulation, and biological consequences of natriuretic peptides and their associated signaling proteins are described.

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Dissertations / Theses on the topic "Natriuretic peptides"

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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
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Books on the topic "Natriuretic peptides"

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Clerico, Aldo, and Michele Emdin, eds. Natriuretic Peptides. Milano: Springer Milan, 2006. http://dx.doi.org/10.1007/88-470-0498-5.

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1937-, Brenner Barry M., and Laragh John H. 1924-, eds. Biologically active atrial peptides. New York, NY: Raven Press, 1987.

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Atrial natriuretic hormones. Englewood Cliffs, NJ: Prentice Hall, 1992.

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Samson, Willis K., and Ellis R. Levin, eds. Natriuretic Peptides in Health and Disease. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3960-4.

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1937-, Brenner Barry M., and Laragh John H. 1924-, eds. Advances in atrial peptide research. New York: Raven Press, 1988.

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Maurice Rapin Colloquia (2nd 1990 Les Baux-de-Provence, France). Atrial natriuretic factor: Physiological and clinical aspects. Paris: Flammarion Médecine-Sciences, 1991.

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Workshop on Cation Transport and Nartriurietic Factors (1985 Cambridge, Mass.). Workshop on Cation Transport and Natriuretic Factors: Cambridge, Massachusetts May 13-14, 1985. Edited by Dzau Victor J, Horan Michael J, Canessa Mitzy, and American Heart Association. [Dallas, Tex.]: American Heart Association, 1987.

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8

American Society of Hypertension. Meeting. First Annual Meeting of the American Society of Hypertension, May 29-30, 1986 ; First World Congress on Biologically Active Atrial Peptides, May 31-June 1, 1986: Program and abstracts, Waldorf-Astoria Hotel, New York, New York. Thorofare, N.J: The Society, 1986.

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F, Mantero, and Vecsei Pál, eds. Corticosteroids and peptide hormones in hypertension. New York: Raven Press, 1987.

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E, Wierman Margaret, ed. Diseases of the pituitary: Diagnosis and treatment. Totowa, N.J: Humana Press, 1997.

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Book chapters on the topic "Natriuretic peptides"

1

Emdin, Michele, Claudio Passino, and Fabio Recchia. "The Heart Complexity The Intrinsic Function (Intrinsic Regulation of Heart Rate and Mechanics)." In Natriuretic Peptides, 7–20. Milano: Springer Milan, 2006. http://dx.doi.org/10.1007/88-470-0498-5_2.

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Lindmark, Krister, and Kurt Boman. "Natriuretic Peptides." In Heart Failure in Clinical Practice, 309–18. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84996-153-0_17.

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Seth, John. "Natriuretic Peptides." In The Immunoassay Kit Directory, 256–64. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1414-1_39.

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Pannu, Neesh, Xiaoyan Wen, John A. Kellum, John Fildes, N. Al-Subaie, Mark Hamilton, Susan M. Lareau, et al. "Natriuretic Peptides." In Encyclopedia of Intensive Care Medicine, 1513. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1922.

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Volpe, Massimo, and Speranza Rubattu. "Natriuretic Peptides." In Updates in Hypertension and Cardiovascular Protection, 87–100. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-93320-7_6.

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Meyer, Markus, Hartmut Lüss, Veselin Mitrovic, and Alexandre Mebazaa. "Natriuretic Peptides." In Acute Heart Failure, 608–20. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-782-4_56.

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Thomson, Neil C. "Atrial Natriuretic Peptides." In Airways Smooth Muscle: Peptide Receptors, Ion Channels and Signal Transduction, 115–29. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7362-8_5.

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Nutt, Ruth F., Terry M. Ciccarone, Stephen F. Brady, C. Dylion Colton, William J. Paleveda, Terry A. Lyle, Theresa M. Williams, Daniel F. Veber, Audrey Wallace, and Raymond J. Winquist. "Structure-activity studies of atrial natriuretic factor." In Peptides, 444–46. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-010-9595-2_130.

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Espiner, Eric A., A. Mark Richards, and M. Gary Nicholls. "Physiology of Natriuretic Peptides." In Endocrinology of Cardiovascular Function, 121–35. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5569-8_7.

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Espiner, Eric A. "Physiology of Natriuretic Peptides." In Natriuretic Peptides in Health and Disease, 123–46. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3960-4_8.

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Conference papers on the topic "Natriuretic peptides"

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Agrawal, V., F. Shi, N. L. Fortune, J. L. Fuentes, E. L. Brittain, S. Collins, J. D. West, and A. Hemnes. "The Natriuretic Peptide Clearance Receptor (NPRC) Promotes Cardiomyocyte Hypertrophy in PH-HFpEF by Endocytosis of Natriuretic Peptides." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6366.

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Tanable, A., Y. Yatomi, T. Ohashi, H. Oka, T. Kariya, and S. Kume. "EFFECTS OF HUMAN ATRIAL NATRIURETIC PEPTIDES ON SECRETION REACTION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644873.

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Abstract:

Human atrial natriuretic peptide (h-ANP) has vasodilating and natriuretic properties, and inhibits smooth muscle contraction, renal renin secretion and adrenal aldosterone release. Although Schiffrin has reported that human platelets have receptors for ANP, its effects in platelets are not established in vivo. We therefore investigated the influence of h-ANP on secretion reaction in human platelets. Eight healthy subjects, males, aged 20 to 24 years, donated blood for the study. Citrated platelet-rich plasma (PRP) was incubated with or without h-ANP at 37 C for 2.5 minutes. The samples of 0.5 ml PRP then used to measure ADP induced aggregation, ATP release reaction and C-serotonin release reaction. H-ANP, at concentration of 1x10 -6M, decreased ADP induced aggregation (after h-ANP: 77.4±9.7 % of control aggregation), and inhibited ATP release reaction (after h-ANP: 31.8±13.1%). Serotonin releasereaction induced by ADP was also inhibited ( control: 15.3±2.2%, after h-ANP: 8.3±0.5 %). The inhibitory effect of h-ANP on aggregation and secretion reaction was maximal by 3 minutes. These data suggest that h-ANP inhibits secretion reaction in human platelets.

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Azzam, Z. S., Y. Knany, S. Kinaneh, E. Khoury, J. Khoury, M. Matan, and Z. Abassi. "Natriuretic Peptides Attenuate the Ability of the Lungs to Clear Edema." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4230.

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Öztop, Mustafa. "Immunohistochemical Distribution of Natriuretic Peptides and Their Receptors in Goat Heart." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-82.

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Kaiser, Ralf, Katharina Grotemeyer, Philip Böhmer, Philipp Lepper, Robert Bals, and Heinrike Wilkens. "Association of haemodynamic parameters with circulating natriuretic peptides in precapillary pulmonary hypertension." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2461.

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Baliga, Reshma S., Chris J. Scotton, Sarah L. Trinder, Rachel C. Chambers, Raymond J. MacAllister, and Adrian J. Hobbs. "Protective Role Of Natriuretic Peptides In Pulmonary Fibrosis: A Novel Therapeutic Target?" In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6409.

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Zheng, Alice, Kaushik Guha, Paul Kalra, and Geraint Morton. "41 Patients with possible heart failure and raised natriuretic peptides have poor outcomes regardless of final diagnosis." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.41.

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Zheng, Alice, Elena Cowan, Legate Philip, Kaushik Guha, Paul R. Kalra, and Geraint Morton. "83 Characteristics and outcomes of patients with suspected heart failure and elevated natriuretic peptides referred to a nice-compliant heart failure clinic." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.81.

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Long, AC, HR O'Neal, Jr, S. Peng, KB Lane, and RW Light. "Comparison of Pleural Fluid N-Terminal Pro-Brain Natriuretic Peptide and Brain Natriuretic-32 Peptide Levels." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4454.

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Ren, Cai-Ling. "Progress of Brain Natriuretic Peptide in Cardiovascular System." In 4th Annual International Conference on Management, Economics and Social Development (ICMESD 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/icmesd-18.2018.35.

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