Journal articles: '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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Wong, Philip Ching Yat, Jun Guo, and Aidong Zhang. "The renal and cardiovascular effects of natriuretic peptides." Advances in Physiology Education 41, no. 2 (June 1, 2017): 179–85. http://dx.doi.org/10.1152/advan.00177.2016.

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The landmark report by de Bold et al. in 1981 signified the heart as one of the endocrine organs involved in fluid and salt balance (de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H. Life Sci 28: 89–94, 1981). Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are secreted from cardiomyocytes in response to cardiac stretch as in the case of heart failure, whereas C-type natriuretic peptide (CNP) is secreted from endothelial and renal cells in response to cytokines and endothelium-dependent agonists, such as acetylcholine. Binding ANP or BNP to natriuretic peptide receptor A induces cyclic guanylyl monophosphate as second messenger in the target cells to mediate the following: natriuresis; water diuresis; increasing glomerular filtration rate; decreasing systemic sympathetic activities; plasma volume; cardiac output and blood pressure; and curbing mitoses of heart fibroblasts and hypertrophy of cardiovascular muscle cells. ANP, BNP, and CNP are cleared from the bloodstream by natriuretic peptide receptor C and degraded by an ectoenzyme called neprilysin (NEP). The plasma levels of BNP are typically >100 pg/ml in patients with congestive heart failure. Sacubitril/valsartan is an angiotensin receptor NEP inhibitor that prevents the clinical progression of surviving patients with heart failure more effectively than enalapril, an angiotensin-converting enzyme inhibitor. A thorough understanding of the renal and cardiovascular effects of natriuretic peptides is of major importance for first-year medical students to gain insight into the significance of plasma levels of BNP in patients with heart failure.

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Tokudome, Takeshi, and Kentaro Otani. "Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide." Biology 11, no. 9 (September 14, 2022): 1351. http://dx.doi.org/10.3390/biology11091351.

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Natriuretic peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), have cardioprotective effects and regulate blood pressure in mammals. ANP and BNP are hormones secreted from the heart into the bloodstream in response to increased preload and afterload. Both hormones act through natriuretic peptide receptor 1 (NPR1). In contrast, CNP acts through natriuretic peptide receptor 2 (NPR2) and was found to be produced by the vascular endothelium, chondrocytes, and cardiac fibroblasts. Based on its relatively low plasma concentration compared with ANP and BNP, CNP is thought to function as both an autocrine and a paracrine factor in the vasculature, bone, and heart. The cytoplasmic domains of both NPR1 and NPR2 display a guanylate cyclase activity that catalyzes the formation of cyclic GMP. NPR3 lacks this guanylate cyclase activity and is reportedly coupled to Gi-dependent signaling. Recently, we reported that the continuous infusion of the peptide osteocrin, an endogenous ligand of NPR3 secreted by bone and muscle cells, lowered blood pressure in wild-type mice, suggesting that endogenous natriuretic peptides play major roles in the regulation of blood pressure. Neprilysin is a neutral endopeptidase that degrades several vasoactive peptides, including natriuretic peptides. The increased worldwide clinical use of the angiotensin receptor-neprilysin inhibitor for the treatment of chronic heart failure has brought renewed attention to the physiological effects of natriuretic peptides. In this review, we provide an overview of the discovery of ANP and its translational research. We also highlight our recent findings on the blood pressure regulatory effects of ANP, focusing on its molecular mechanisms.

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Ghosh, Nina, and Haissam Haddad. "Atrial natriuretic peptides in heart failure: pathophysiological significance, diagnostic and prognostic value." Canadian Journal of Physiology and Pharmacology 89, no. 8 (August 2011): 587–91. http://dx.doi.org/10.1139/y11-040.

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Neurohormonal activation in patients with heart failure is dominated by the deleterious long-term effects of activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system. The natriuretic peptides, including brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP), are also upregulated in heart failure, and partially counteract these deleterious effects by promoting vasodilation, natriuresis, and diuresis. Although BNP has been established as an important biomarker in the diagnosis and prognosis of heart failure, growing evidence suggests that measurement of plasma ANP, specifically its metabolite mid-regional pro-ANP, has similar diagnostic and prognostic value. Furthermore, its measurement may provide incremental diagnostic value when BNP levels fall into “grey zone” levels and may be a more potent prognostic marker of mortality.

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Cataliotti, Alessandro, and John C. Burnett. "Natriuretic Peptides." Journal of Investigative Medicine 53, no. 7 (November 2005): 378–84. http://dx.doi.org/10.2310/6650.2005.53711.

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Stoupakis, George, and Marc Klapholz. "Natriuretic Peptides." Heart Disease 5, no. 3 (May 2003): 215–23. http://dx.doi.org/10.1097/01.hdx.0000074517.30102.64.

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Arulkumaran, Nishkantha, and John R. Prowle. "Natriuretic Peptides." Anesthesiology 129, no. 2 (August 1, 2018): 235–37. http://dx.doi.org/10.1097/aln.0000000000002307.

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Giovannelli, Francesca, Fabiana Piccioni, Massimo Volpe, and Speranza Rubattu. "Natriuretic Peptides." High Blood Pressure & Cardiovascular Prevention 12, no. 4 (2005): 215–23. http://dx.doi.org/10.2165/00151642-200512040-00003.

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Epstein, Franklin H., Ellis R. Levin, David G. Gardner, and Willis K. Samson. "Natriuretic Peptides." New England Journal of Medicine 339, no. 5 (July 30, 1998): 321–28. http://dx.doi.org/10.1056/nejm199807303390507.

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Daniels, Lori B., and Alan S. Maisel. "Natriuretic Peptides." Journal of the American College of Cardiology 50, no. 25 (December 2007): 2357–68. http://dx.doi.org/10.1016/j.jacc.2007.09.021.

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Boerrigter, Guido, and John C. Burnett. "Natriuretic Peptides." Journal of the American College of Cardiology 58, no. 9 (August 2011): 904–6. http://dx.doi.org/10.1016/j.jacc.2010.12.053.

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Richards, A. Mark, M. Gary Nicholls, and Eric A. Espiner. "Natriuretic Peptides." Clinical Science 88, no. 1 (January 1, 1995): 18–21. http://dx.doi.org/10.1042/cs0880018.

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Richards, A. Mark. "Natriuretic Peptides." Hypertension 50, no. 1 (July 2007): 25–30. http://dx.doi.org/10.1161/hypertensionaha.106.069153.

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Wigle, D. A., B. M. Bennett, D. B. Jennings, I. R. Sarda, T. G. Flynn, and S. C. Pang. "Biological effects of rat iso-atrial natriuretic peptide and brain natriuretic peptide are indistinguishable from each other." Canadian Journal of Physiology and Pharmacology 70, no. 11 (November 1, 1992): 1525–28. http://dx.doi.org/10.1139/y92-218.

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Rat brain natriuretic peptide (rBNP) and iso-atrial natriuretic peptide (iso-rANP) were discovered independently by two research laboratories. They are considered to be members of the B-type natriuretic peptides. Except for the Gln/Leu substitution at position 44, the amino acid sequence of iso-rANP is identical with that of the C-terminal 45 amino acids of rat pro-BNP and with the 5-kDa cardiac peptide from rat atria. To determine whether this amino acid substitution can modify the known biological effects of rBNP and iso-rANP, the present investigation examined the cardiovascular and renal responses, vasorelaxant effect, receptor binding characteristics, and cyclic GMP production by the two peptides in relation to that of rat atrial natriuretic peptide (rANP). Results indicate that rBNP and iso-rANP are indistinguishable from each other in terms of these known biological activities of atrial natriuretic peptide. We therefore conclude that rBNP and iso-rANP are identical peptides and that the amino acid substitution at position 44 represents a polymorphic form of the rat B-type natriuretic peptide.Key words: atrial natriuretic peptide, brain natriuretic peptide, cardiovascular response, vasorelaxation, cyclic GMP, receptor binding.

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Vesely, David L. "Natriuretic peptides and acute renal failure." American Journal of Physiology-Renal Physiology 285, no. 2 (August 2003): F167—F177. http://dx.doi.org/10.1152/ajprenal.00259.2002.

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Atrial natriuretic peptides (ANPs) are a family of peptide hormones, e.g., ANP, long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide synthesized by the ANP gene. Brain natriuretic peptide (BNP) and C-type natriuretic peptide are also members of this family but are synthesized by separate genes. Within the kidney, the ANP prohormone's posttranslational processing is different from that of other tissues, resulting in an additional four amino acids added to the NH2terminus of ANP (e.g., urodilatin). Each of these natriuretic and diuretic peptides increases within the circulation with acute renal failure (ARF). Renal transplantation but not hemodialysis returns their circulating concentrations to those of healthy individuals. BNP and adrenomedullin, a 52-amino acid natriuretic peptide, have beneficial effects on glomerular hypertrophy and glomerular injury but do not improve tubular injury (i.e., acute tubular necrosis). Vessel dilator ameliorates acute tubular necrosis with regeneration of the brush borders of proximal tubules. Vessel dilator decreases mortality in ARF from 88 to 14% at day 6 of ARF, even when given 2 days after renal failure has been established.

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VILLA, Giorgio LA, Massimo MANNELLI, Chiara LAZZERI, Sabrina VECCHIARINO, Maria Laura DE FEO, Cristina TOSTI GUERRA, Renzo BANDINELLI, Marco FOSCHI, and Franco FRANCHI. "Different effects of atrial and C-type natriuretic peptide on the urinary excretion of endothelin-1 in man." Clinical Science 95, no. 5 (November 1, 1998): 595–602. http://dx.doi.org/10.1042/cs0950595.

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1.Following the observation that brain natriuretic peptide enhances the urinary excretion rate of endothelin-1, the relationship between natriuretic peptides and urinary endothelin-1 was further investigated. Six healthy volunteers received, on three different occasions, increasing doses of atrial or C-type natriuretic peptide (0, 2 and 4 ;pmol·min-1·kg-1 for 1 ;h each), or placebo. 2.Atrial natriuretic peptide caused significant increases in the urinary excretion of cGMP, sodium and endothelin-1, without affecting plasma endothelin-1, renal plasma flow, glomerular filtration rate and urine flow rate. C-type natriuretic peptide did not modify any of these parameters. During atrial natriuretic peptide infusion, urinary endothelin-1 directly correlated with plasma atrial natriuretic peptide, urinary cGMP and sodium excretion. 3.These results indicate that enhancement of the urinary excretion of endothelin-1 by natriuretic peptides is dose-dependent and somewhat related to their ability to bind to natriuretic peptide receptors A, activate guanylate cyclase and induce a natriuretic response.

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Savoia, Carmine, Massimo Volpe, Alessandro Alonzo, Chiara Rossi, and Speranza Rubattu. "Natriuretic peptides and cardiovascular damage in the metabolic syndrome: molecular mechanisms and clinical implications." Clinical Science 118, no. 4 (November 9, 2009): 231–40. http://dx.doi.org/10.1042/cs20090204.

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Natriuretic peptides are endogenous antagonists of vasoconstrictor and salt- and water-retaining systems in the body's defence against blood pressure elevation and plasma volume expansion, through direct vasodilator, diuretic and natriuretic properties. In addition, natriuretic peptides may play a role in the modulation of the molecular mechanisms involved in metabolic regulation and cardiovascular remodelling. The metabolic syndrome is characterized by visceral obesity, hyperlipidaemia, vascular inflammation and hypertension, which are linked by peripheral insulin resistance. Increased visceral adiposity may contribute to the reduction in the circulating levels of natriuretic peptides. The dysregulation of neurohormonal systems, including the renin–angiotensin and the natriuretic peptide systems, may in turn contribute to the development of insulin resistance in dysmetabolic patients. In obese subjects with the metabolic syndrome, reduced levels of natriuretic peptides may be involved in the development of hypertension, vascular inflammation and cardio vascular remodelling, and this may predispose to the development of cardiovascular disease. The present review summarizes the regulation and function of the natriuretic peptide system in obese patients with the metabolic syndrome and the involvement of altered bioactive levels of natriuretic peptides in the pathophysiology of cardiovascular disease in patients with metabolic abnormalities.

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Tanase, Daniela Maria, Smaranda Radu, Sinziana Al Shurbaji, Genoveva Livia Baroi, Claudia Florida Costea, Mihaela Dana Turliuc, Anca Ouatu, and Mariana Floria. "Natriuretic Peptides in Heart Failure with Preserved Left Ventricular Ejection Fraction: From Molecular Evidences to Clinical Implications." International Journal of Molecular Sciences 20, no. 11 (May 28, 2019): 2629. http://dx.doi.org/10.3390/ijms20112629.

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The incidence of heart failure with preserved ejection fraction (HFpEF) is increasing and its challenging diagnosis and management combines clinical, imagistic and biological data. Natriuretic peptides (NPs) are hormones secreted in response to myocardial stretch that, by increasing cyclic guanosine monophosphate (cGMP), counteract myocardial fibrosis and hypertrophy, increase natriuresis and determine vasodilatation. While their role in HFpEF is controversial, most authors focused on b-type natriuretic peptides (BNPs) and agreed that patients may show lower levels. In this setting, newer molecules with an increased specificity, such as middle-region pro-atrial natriuretic peptide (MR-proANP), emerged as promising markers. Augmenting NP levels, either by NP analogs or breakdown inhibition, could offer a new therapeutic target in HFpEF (already approved in their reduced EF counterparts) by increasing the deficient cGMP levels found in patients. Importantly, these peptides also retain their prognostic value. This narrative review focuses on NPs’ physiology, diagnosis, therapeutic and prognostic implication in HFpEF.

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Vasile, Vlad C., and Allan S. Jaffe. "Natriuretic Peptides and Analytical Barriers." Clinical Chemistry 63, no. 1 (January 1, 2017): 50–58. http://dx.doi.org/10.1373/clinchem.2016.254714.

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Abstract BACKGROUND The natriuretic peptide system is an endocrine, autocrine and paracrine system that plays an important role in the maintenance of cardiovascular homeostasis. Biomarkers based on these peptides are important diagnostic and prognostic tools for myocardial function. CONTENT Although natriuretic peptides were discovered more than 2 decades ago, their intricate and complex biology is associated with important questions not yet elucidated. The diversity of circulating forms of natriuretic peptides, the distinct expression of these forms in particular patients, and the heterogeneity of heart failure forms, along with specific assay-related and preanalytic issues, cause assays to be poorly harmonized. SUMMARY This review presents the relevant issues related to the biology of natriuretic peptides and differences between assays with immediate implications for clinical practice.

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Cozza, Eduardo N., Mark F. Foecking, Maria del Carmen Vila, and Celso E. Gomez-Sanchez. "Adrenal receptors for natriuretic peptides and inhibition of aldosterone secretion in calf zona glomerulosa cells in culture." Acta Endocrinologica 129, no. 1 (July 1993): 59–64. http://dx.doi.org/10.1530/acta.0.1290059.

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Atrial and brain natriuretic peptides specifically bind to primary cultures of calf adrenal glomerulosa cells. Binding of both natriuretic peptides to the same receptor has been proved by: a Dixon plot showing competitive effects for the binding of 125I-labeled brain natriuretic peptide in the presence of increasing concentrations of unlabeled atrial natriuretic peptide; a Scatchard plot showing a lower dissociation constant (Kd) for atrial natriuretic peptide than for brain natriuretic peptide binding, but the maximum binding (Bmax) values were the same; autoradiography of sodium dodecyl sulfate polyacrylamide gels after cross-linking of 125I-labeled atrial natriuretic peptide and 125I-labeled brain natriuretic peptide, showing the same molecular weights for both peptide receptors—a single 66-kD band in whole cells and a main band at 125 kD in membranes. C-Type atrial natriuretic peptide only slightly displaced atrial natriuretic peptide binding. Angiotensin II- and potassium-mediated stimulation of aldosterone production were inhibited strongly and to the same degree by atrial and brain natriuretic peptide but only slightly by C-type atrial natriuretic peptide. Stimulation of aldosterone production mediated by adrenocorticotropin was only partially inhibited by atrial and brain natriuretic peptide, while baseline aldosterone was not affected. These results suggest that atrial and brain natriuretic peptide bind to the same receptors and provoke the same effects on aldosterone production. The weak effects found with C-type atrial natriuretic peptide suggest that the primary culture of calf adrenal glomerulosa cells contain the guanylate cyclase A receptor.

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Dunn, Michael E., Thomas G. Manfredi, Kevin Agostinucci, Steven K. Engle, Josh Powe, Nicholas M. P. King, Luis A. Rodriguez, et al. "Serum Natriuretic Peptides as Differential Biomarkers Allowing for the Distinction between Physiologic and Pathologic Left Ventricular Hypertrophy." Toxicologic Pathology 45, no. 2 (July 11, 2016): 344–52. http://dx.doi.org/10.1177/0192623316634231.

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Given the proven utility of natriuretic peptides as serum biomarkers of cardiovascular maladaptation and dysfunction in humans and the high cross-species sequence conservation of atrial natriuretic peptides, natriuretic peptides have the potential to serve as translational biomarkers for the identification of cardiotoxic compounds during multiple phases of drug development. This work evaluated and compared the response of N-terminal proatrial natriuretic peptide (NT-proANP) and N-terminal probrain natriuretic peptide (NT-proBNP) in rats during exercise-induced and drug-induced increases in cardiac mass after chronic swimming or daily oral dosing with a peroxisome proliferator-activated receptor γ agonist. Male Sprague-Dawley rats aged 8 to 10 weeks were assigned to control, active control, swimming, or drug-induced cardiac hypertrophy groups. While the relative heart weights from both the swimming and drug-induced cardiac hypertrophy groups were increased 15% after 28 days of dosing, the serum NT-proANP and NT-proBNP values were only increased in association with cardiac hypertrophy caused by compound administration. Serum natriuretic peptide concentrations did not change in response to adaptive physiologic cardiac hypertrophy induced by a 28-day swimming protocol. These data support the use of natriuretic peptides as fluid biomarkers for the distinction between physiological and drug-induced cardiac hypertrophy.

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Vesely, D. L., S. Chiou, M. A. Douglass, M. T. McCormick, G. Rodriguez-Paz, and D. D. Schocken. "Kaliuretic peptide and long acting natriuretic peptide as well as atrial natriuretic factor inhibit aldosterone secretion." Journal of Endocrinology 146, no. 3 (September 1995): 373–80. http://dx.doi.org/10.1677/joe.0.1460373.

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Abstract The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1–30 (long acting natriuretic peptide), 31–67 (vessel dilator) and 79–98 (kaliuretic peptide) as well as 99–126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P<0·001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P<0·01) decreased plasma aldosterone levels which remained significantly (P<0·001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P<0·01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P<0·001) than following ANF infusion. Journal of Endocrinology (1995) 146, 373–380

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Ichiki, Tomoko, Atsushi Jinno, and Yoshihisa Tsuji. "Natriuretic Peptide-Based Novel Therapeutics: Long Journeys of Drug Developments Optimized for Disease States." Biology 11, no. 6 (June 3, 2022): 859. http://dx.doi.org/10.3390/biology11060859.

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The field of natriuretic peptides (NPs) as an endocrine hormone has been developing since 1979. There are three peptides in humans: atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), which bind to the guanylyl cyclase-A (GC-A) receptor (also called natriuretic peptide receptor-A (NPR-A)), and C-type natriuretic peptide (CNP), which binds to the GC-B receptor (also called the NPR-B) and then synthesizes intracellular cGMP. GC-A receptor stimulation has natriuretic, vasodilatory, cardiorenal protective and anti-renin–angiotensin–aldosterone system actions, and GC-B receptor stimulation can suppress myocardial fibrosis and can activate bone growth before epiphyseal plate closure. These physiological effects are useful as therapeutics for some disease states, such as heart failure, hypertension, and dwarfism. To optimize the therapeutics for each disease state, we must consider drug metabolism, delivery systems, and target receptor(s). We review the cardiac NP system; new designer NPs, such as modified/combined NPs and modified peptides that can bind to not only NP receptors but receptors for other systems; and oral drugs that enhance endogenous NP activity. Finally, we discuss prospective drug discoveries and the development of novel NP therapeutics.

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Zakeri, Rosita, and John C. Burnett. "Designer natriuretic peptides: a vision for the future of heart failure therapeutics." Canadian Journal of Physiology and Pharmacology 89, no. 8 (August 2011): 593–601. http://dx.doi.org/10.1139/y11-048.

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Despite recent pharmacological advances in heart failure therapy, mortality from acute decompensated heart failure remains high. Conventional therapies are often insufficient to address the complex interplay between structural, functional, neurohumoral, and renal mechanisms involved in the heart failure syndrome. The natriuretic peptide system, however, offers a unique pleiotropic strategy which could bridge this gap in heart failure therapy. Exogenous administration of native A-type and B-type natriuretic peptides has been met with both success and limitations, and despite the limitations, remains a worthwhile endeavor. Alternatively, synthetic modification to create “designer” chimeric peptides holds the possibility to extend both the application and therapeutic benefits possible with a natriuretic peptide based approach. Herein we describe the development of natriuretic peptide based heart failure therapies, including the design, rationale, and preliminary studies of the novel chimeric peptides CD-NP and CU-NP.

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Fonteles, Manassés Claudino, and Nilberto Robson Falcão do Nascimento. "Guanylin peptide family: history, interactions with ANP, and new pharmacological perspectives." Canadian Journal of Physiology and Pharmacology 89, no. 8 (August 2011): 575–85. http://dx.doi.org/10.1139/y11-050.

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The guanylin family of peptides has 3 subclasses of peptides containing either 3 intramolecular disulfide bonds found in bacterial heat-stable enterotoxins (ST), or 2 disulfides observed in guanylin and uroguanylin, or a single disulfide exemplified by lymphoguanylin. These peptides bind to and activate cell-surface receptors that have intrinsic guanylate cyclase (GC) activity. These hormones are synthesized in the intestine and released both luminally and into the circulation, and are also produced within the kidney. Stimulation of renal target cells by guanylin peptides in vivo or ex vivo elicits a long-lived diuresis, natriuresis, and kaliuresis by both cGMP-dependent and independent mechanisms. Uroguanylin may act as a hormone in a novel endocrine axis linking the digestive system and kidney as well as a paracrine system intrarenally to increase sodium excretion in the postprandial period. This highly integrated and redundant mechanism allows the organism to maintain sodium balance by eliminating excess sodium in the urine. In addition, small concentrations of the atrial natriuretic peptide (ANP) can synergize with low concentrations of both guanylin or uroguanylin, which do not induce natriuresis per se, to promote significant natriuresis. Interestingly, the activation of the particulate guanylate cyclase receptors by natriuretic peptides can promote relaxation of animal and human penile erectile tissue and increase intracavernosal pressure to induce penile erection. These peptides can be prototypes for new drugs to treat erectile dysfunction, especially in patients with endothelial and nitrergic dysfunction, such as in diabetes.

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Goetze, Jens P. "B-Type Natriuretic Peptide: From Posttranslational Processing to Clinical Measurement." Clinical Chemistry 58, no. 1 (January 1, 2012): 83–91. http://dx.doi.org/10.1373/clinchem.2011.165696.

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Abstract BACKGROUND Plasma cardiac natriuretic peptides and peptide fragments from their molecular precursors are markers of heart disease. Clinical studies have defined the current diagnostic utility of these markers, whereas biochemical elucidation of peptide structure and posttranslational processing has revealed new plasma peptide forms of potential clinical use. CONTENT Natriuretic propeptide structures undergo variable degrees of endo- and exoproteolytic cleavages as well as amino acid modifications, which leave the plasma phase of the peptides highly heterogeneous and dependent on cardiac pathophysiology and capacity. An ongoing characterization of the molecular heterogeneity may not only help us to appreciate the biosynthetic capacity of the endocrine heart but may also lead to the discovery of new and more disease-specific targets for future molecular diagnosis. SUMMARY Peptides derived from pro–atrial natriuretic peptide and pro–B-type natriuretic peptide are useful plasma markers in heart failure. New data have defined cardiac myocytes as competent endocrine cells in posttranslational processing and cellular secretion.

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Bajric, Mugdim, Fahir Barakovic, Nusret Sinanovic, and Denis Mrsic. "CLINICAL USE OF NATRIURETIC PEPTIDES. A REVIEW." Acta Medica Saliniana 37, no. 2 (December 28, 2008): 174–79. http://dx.doi.org/10.5457/ams.v37i2.19.

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The most significant discoveries in the area of heart failure are the recognition of natriuretic peptide system and its multiple effects on cardiac structure and function with special effect on its natriuretic and hemodynamic processes. First information’s that heart, beside its function as a mechanical pump also has an important endocrine functions, exists for over 50 years. Chemical structure of atrial natriuretic peptide has been identified in 1984. and four years later a brain natriuretic peptide has been discovered owning its name because it has been identified in pig brain. Primary site of brain natriuretic peptide synthesis in heart has been identified in 1991. Natriuretic peptides are neither neurohormones that influence body fluid homeostasis through natriuretic and diuretic effect; regulate vascular tone by decreasing angiotensine II level and they inhibit nor epinephrine synthesis and increase parasympathetic tone. They are natural antagonists of renin-angiotensine-aldosteron system, and they have a great role in inhibition of ventricular hypertrophy and remodeling, protective effects in endothelial dysfunction are important; they increase effects of nitrite oxide, inhibit lipid deposition in vascular wall and inhibit thrombocyte activation, regulate coagulation and fibrinolytic processes as well. Natriuretic peptides clinical use is in early evaluation of heart failure, prognostic stratification and detection of systolic and diastolic dysfunction of left ventricle, assessment of prognosis during patient monitoring period, differential diagnosis of dyspnea, treatment adjustment and dosage titration, assessment during hospital admittance and discharge and forecast and reduction of coronary events.

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Saidova, V. T. "Diagnostic value of natriuretic peptides in pediatrics." Kazan medical journal 94, no. 3 (June 15, 2013): 350–54. http://dx.doi.org/10.17816/kmj2183.

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Natriuretic peptide hormones are the family of vasoactive substanses produced by cardiomyocytes in response to the expansion and increased pressure in the heart chambers. The review of the literature focuses on the diagnostic role of natriuretic peptides in pediatrics. The most important clinical effects of natriuretic peptides, brief history of their discovery and studying, age-related changes of serum levels are analyzed. Data of their use in the diagnosis and cardiac function monitoring in various forms of cardiomyopathy, myocardial inflammatory diseases, Kawasaki disease in children are presented. The results of studies examining the natriuretic peptides levels in children with congenital heart defects and heart transplantation in pre-and postoperative period are reviewed. The review involved the diagnostic use of natriuretic peptides in neonates, including high pulmonary hypertension and hemodynamically significant patent ductus arteriosus diagnosis in preterm infants. The possibility of the natriuretic peptides use for assessing the cardiotoxic complications risk in anti-tumor chemotherapy and for differential diagnosis of acute dyspnea due to heart failure or pulmonary diseases are discussed.

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Nigwekar, Sagar U., Hrishikesh Kulkarni, and Charuhas V. Thakar. "Natriuretic Peptides in the Management of Solid Organ Transplantation Associated Acute Kidney Injury: A Systematic Review and Meta-Analysis." International Journal of Nephrology 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/949357.

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Randomized controlled trials involving natriuretic peptide administration in solid organ transplantation setting have shown inconsistent effects for renal endpoints. We conducted a systematic review and meta-analysis of these trials to ascertain the role of natriuretic peptides in the management of solid organ transplantation associated acute kidney injury (AKI). MEDLINE, EMBASE, and Google scholar were searched independently by two authors for randomized trials evaluating renal effects of natriuretic peptides in solid organ transplantation settings. Two reviewers independently assessed the studies for eligibility and extracted the relevant data. The pooled estimate showed that natriuretic peptide administration is associated with a reduction in AKI requiring dialysis (odds ratio = 0.50 [0.26–0.97]), a statistically nonsignificant trend toward improvement in posttransplant creatinine clearance (weighted mean difference = 5.5 mL/min, [−1.3 to 12.2 mL/min]), and reduction in renal replacement requirement duration (weighted mean difference −44.0 hours, [−60.5 to −27.5 hours]). There were no mortality events and no adverse events related to natriuretic peptides. In conclusion, administration of natriuretic peptides in solid organ transplantation may be associated with significant improvements in renal outcomes. These observations need to be confirmed in an adequately powered, prospective multicenter study.

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Clerico, Aldo, Alberto Giannoni, Simona Vittorini, and Claudio Passino. "Thirty years of the heart as an endocrine organ: physiological role and clinical utility of cardiac natriuretic hormones." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 1 (July 2011): H12—H20. http://dx.doi.org/10.1152/ajpheart.00226.2011.

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Thirty years ago, De Bold et al. ( 20 ) reported that atrial extracts contain some biologically active peptides, which promote a rapid and massive diuresis and natriuresis when injected in rats. It is now clear that the heart also exerts an endocrine function and in this way plays a key role in the regulation of cardiovascular and renal systems. The aim of this review is to discuss some recent insights and still-debated findings regarding the cardiac natriuretic hormones (CNHs) produced and secreted by cardiomyocytes (i.e., atrial natriuretic peptide and B-type natriuretic peptide). The functional status of the CNH system depends not only on the production/secretion of CNHs by cardiomyocytes but also on both the peripheral activation of circulating inactive precursor of natriuretic hormones and the transduction of the hormone signal by specific receptors. In this review, we will discuss the data supporting the hypothesis that the production and secretion of CNHs is the result of a complex integration among mechanical, chemical, hemodynamic, humoral, ischemic, and inflammatory inputs. The cross talk among endocrine function, adipose tissue, and sex steroid hormones will be discussed more in detail, considering the clinically relevant relationships linking together cardiovascular risk, sex, and body fat development and distribution. Finally, we will review the pathophysiological role and the clinical relevance of both peripheral maturation of the precursor of B-type natriuretic peptides and hormone signal transduction .

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Kenny, A. J., A. Bourne, and J. Ingram. "Hydrolysis of human and pig brain natriuretic peptides, urodilatin, C-type natriuretic peptide and some C-receptor ligands by endopeptidase-24.11." Biochemical Journal 291, no. 1 (April 1, 1993): 83–88. http://dx.doi.org/10.1042/bj2910083.

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Endopeptidase-24.11 (E-24.11, EC 3.4.24.11) is widely believed to play a physiological role in metabolizing atrial natriuretic peptide (ANP). Since the discovery of ANP, new natriuretic peptides have been isolated and other peptides synthesized as receptor ligands. The hydrolysis in vitro of six related peptides by the endopeptidase has been studied, mainly by h.p.l.c. The initial attack on the 32-residue form of pig brain natriuretic peptide (pBNP-32) was shown to be at the Ser20-Leu21 bond, as had been previously shown for the 26-residue form. In contrast, human brain natriuretic peptide-32 (hBNP-32), which differs in ten residues from pBNP-32, was attacked first at the Met4-Val5 bond, releasing the N-terminal tetrapeptide, and only later at bonds within the ring: at Arg17-Ile18 and subsequently at four other sites. Urodilatin, which has a four-residue extension at the N-terminus compared with alpha-human atrial natriuretic peptide-28 (alpha-hANP), was degraded at about half the rate of the latter, though the C-terminal Phe-Arg-Tyr was released at the same rate. The 22-residue C-type natriuretic peptide was hydrolysed more rapidly than alpha-hANP, as were two C-receptor ligands (peptides with deletions within the ring): C-ANP4-23 (rANP4-23 des-Gln18,Ser19,Gly20,Leu21,Gly22) and SC 46542 (hANP5-28 des-Phe8,Gly9,Ala17,Gln18). Angiotensin-converting enzyme failed to hydrolyse pBNP-32, hBNP-32 or 125I-rat (r) ANP, even after prolonged incubation. Km and kcat values were determined for the hydrolysis of alpha-hANP, porcine BNP-26, porcine BNP-32 and 125I-rANP by E-24.11. Ki values were determined for six peptides, alpha-hANP, urodilatin, hBNP-32, C-type natriuretic peptide (CNP), SC 46542 and C-type natriuretic peptide (C-ANP4-23), in radiometric assays of E-24.11 with either [125I] insulin B chain or [125I] rANP as substrate. The Ki values (2.5-13 microM) for CNP were the lowest of any of the group, whereas those for hBNP-32 (151-172 microM) were the highest. The physiological significance of these results is discussed, especially in regard to the relative resistance of hBNP-32 to attack and the ability of the C-receptor ligands to compete with natriuretic peptides for hydrolysis by E-24.11.

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NG, L. L., S. GEERANAVAR, S. C. JENNINGS, I. LOKE, and R. J. O'BRIEN. "Diagnosis of heart failure using urinary natriuretic peptides." Clinical Science 106, no. 2 (February 1, 2004): 129–33. http://dx.doi.org/10.1042/cs20030234.

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In the present study, we assessed the use of urinary natriuretic peptides [N-terminal proatrial natriuretic peptide (N-ANP) and N-terminal pro-brain natriuretic peptide (N-BNP) and C-type natriuretic peptide (CNP)] in the diagnosis of heart failure. Thirty-four consecutive hospitalized heart failure patients (median age, 75.5 years; 14 female) were compared with 82 age- and gender-matched echocardiographically normal controls. All subjects provided plasma and urine specimens. Plasma was assayed for N-BNP, and urine was assayed for N-ANP, N-BNP and CNP. The diagnostic efficiency of peptides was assessed using receiver operating characteristic (ROC) curve analysis. All three urinary natriuretic peptides were significantly elevated in heart failure patients (P<0.001). Urine N-BNP was correlated with plasma N-BNP (rs=0.53, P<0.0005). Areas under the ROC curves for urinary N-ANP, N-BNP and CNP were 0.86, 0.93 and 0.70 and for plasma N-BNP was 0.96. Correcting urinary peptide levels using urine creatinine produced ROC areas of 0.89, 0.93 and 0.76 respectively. A urine N-BNP level cut-off point of 11.6 fmol/ml had a sensitivity and specificity for heart failure detection of 97% and 78% respectively, with positive and negative predictive values of 64.7 and 98%. In conclusion, although all three natriuretic peptides were elevated in urine in heart failure, urinary N-BNP had diagnostic accuracy comparable with plasma N-BNP. Use of urinary N-BNP for heart failure diagnosis may be suitable for high-throughput screening, especially in subjects reluctant to provide blood samples.

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Kitamura, Hiroaki, Daisuke Nakano, Yoshiharu Sawanobori, Takehiko Asaga, Hideki Yokoi, Motoko Yanagita, Masashi Mukoyama, et al. "Guanylyl Cyclase A in Both Renal Proximal Tubular and Vascular Endothelial Cells Protects the Kidney against Acute Injury in Rodent Experimental Endotoxemia Models." Anesthesiology 129, no. 2 (August 1, 2018): 296–310. http://dx.doi.org/10.1097/aln.0000000000002214.

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Abstract What We Already Know about This Topic What This Article Tells Us That Is New Background Natriuretic peptides are used, based on empirical observations, in intensive care units as antioliguric treatments. We hypothesized that natriuretic peptides prevent lipopolysaccharide-induced oliguria by activating guanylyl cyclase A, a receptor for natriuretic peptides, in proximal tubules and endothelial cells. Methods Normal Sprague-Dawley rats and mice lacking guanylyl cyclase A in either endothelial cells or proximal tubular cells were challenged with lipopolysaccharide and assessed for oliguria and intratubular flow rate by intravital imaging with multiphoton microscopy. Results Recombinant atrial natriuretic peptide efficiently improved urine volume without changing blood pressure after lipopolysaccharide challenge in rats (urine volume at 4 h, lipopolysaccharide: 0.6 ± 0.3 ml · kg−1 · h−1; lipopolysaccharide + fluid resuscitation: 4.6 ± 2.0 ml · kg−1 · h−1; lipopolysaccharide + fluid resuscitation + atrial natriuretic peptide: 9.0 ± 4.8 ml · kg−1 · h−1; mean ± SD; n = 5 per group). Lipopolysaccharide decreased glomerular filtration rate and slowed intraproximal tubular flow rate, as measured by in vivo imaging. Fluid resuscitation restored glomerular filtration rate but not tubular flow rate. Adding atrial natriuretic peptide to fluid resuscitation improved both glomerular filtration rate and tubular flow rate. Mice lacking guanylyl cyclase A in either proximal tubules or endothelium demonstrated less improvement of tubular flow rate when treated with atrial natriuretic peptide, compared with control mice. Deletion of endothelial, but not proximal tubular, guanylyl cyclase A augmented the reduction of glomerular filtration rate by lipopolysaccharide. Conclusions Both endogenous and exogenous natriuretic peptides prevent lipopolysaccharide-induced oliguria by activating guanylyl cyclase A in proximal tubules and endothelial cells.

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LAINCHBURY, J. G., M. G. NICHOLLS, E. A. ESPINER, H. IKRAM, T. G. YANDLE, and A. M. RICHARDS. "Regional plasma levels of cardiac peptides and their response to acute neutral endopeptidase inhibition in man." Clinical Science 95, no. 5 (November 1, 1998): 547–55. http://dx.doi.org/10.1042/cs0950547.

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1.The cardiac natriuretic peptides, atrial natriuretic peptide and brain natriuretic peptide, are degraded via clearance receptors and the enzyme neutral endopeptidase (EC 3.4.24.11). We studied the regional plasma concentrations of these peptides and their response to acute neutral endopeptidase inhibition in a consecutive series of patients with a broad spectrum of severity of cardiac dysfunction who were undergoing diagnostic right and left heart catheterization (24 patients, mean age 62.6 years). 2.Baseline blood samples were obtained for hormone analysis from femoral artery, femoral vein, renal vein, hepatic vein, superior vena cava, coronary sinus and pulmonary artery, and initial haemodynamic measurements were made. Twelve patients then received a neutral endopeptidase inhibitor (SCH 32615, 200 ;mg intravenously) and 12 received vehicle alone. The cardiac catheterization procedure was then completed and haemodynamic and hormone measurements were repeated. 3.Haemodynamic status was similar at baseline in both groups, and at repeated measurement (post-procedure after placebo or active drugs) haemodynamic variables were not significantly different from baseline values. Plasma levels of atrial and brain natriuretic peptides exhibited an arteriovenous increment (344% and 124% respectively) across the heart (femoral artery to coronary sinus) and decrement (by 28–54% and 9–16% respectively) across all other tissue beds (P< 0.05 for all) except the lung (no change). Final levels of atrial natriuretic peptide rose above initial levels at all sites in both groups (P< 0.05) except coronary sinus levels in the vehicle group (no change). The increase was consistently greater in the inhibitor group at all sites (P< 0.05 versus placebo). Levels of brain natriuretic peptide rose at all sites in the inhibitor group only (P< 0.05). The transcardiac step-up in atrial natriuretic peptide was markedly augmented after the administration of neutral endopeptidase inhibitor. Other tissue gradients were not significantly altered by neutral endopeptidase inhibitor. 4.Atrial and brain natriuretic peptides in plasma are degraded by a number of tissues, and respond differently to cardiac catheterization. Neutral endopeptidase has a significant role in determining plasma levels of natriuretic peptides, in part perhaps by influencing the amount of intact peptide reaching the circulation after secretion from the heart.

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Itoh, H., N. Sagawa, M. Hasegawa, T. Mori, S. Suga, M. Mukoyama, T. Yoshimasa, H. Itoh, and K. Nakao. "Umbilical venous guanosine 3',5'-cyclic phosphate (cGMP) concentration increases in asphyxiated newborns." Reproduction, Fertility and Development 7, no. 6 (1995): 1515. http://dx.doi.org/10.1071/rd9951515.

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Guanosine 3',5'-cyclic phosphate (cGMP) is known to be the second messenger of natriuretic peptides and nitric oxide (NO). To investigate the involvement of natriuretic peptides in the regulation of the feto-placental circulation, specific radioimmunoassays were used to measure the concentrations of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and cGMP in the umbilical venous plasma of normal and asphyxiated newborns. The plasma concentrations of ANP, BNP and cGMP in asphyxiated newborns were 48.3 +/- 12.9 pm, 24.5 +/- 9.4 pm and 4.4 +/- 1.6 nM (mean +/- s.e.m., n = 10), respectively. These values were significantly higher than those in the normal newborns (17.4 +/- 1.9 pm, 4.7 +/- 1.0 pm, and 0.78 +/- 0.14 nM, respectively). Moreover, the expression of both ANP-A and ANP-B receptor, biologically active receptors for natriuretic peptides, was detected in term human placenta by Northern bolt analysis. The expression of natriuretic peptide receptors was further confirmed by binding assay using [125I]-labelled ANP and solubilized crude membrane preparations of placental tissue. These findings suggest that cGMP is produced in the placenta, at least partly, by the action of ANP and BNP secreted from fetal heart, in pathophysiological conditions such as fetal hypoxia.

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Charles, C. J., E. A. Espiner, A. M. Richards, M. G. Nicholls, and T. G. Yandle. "Comparative bioactivity of atrial, brain, and C-type natriuretic peptides in conscious sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 6 (June 1, 1996): R1324—R1331. http://dx.doi.org/10.1152/ajpregu.1996.270.6.r1324.

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Although atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) appear to share functional homology, there is doubt concerning a possible endocrine function for C-type natriuretic peptide (CNP) and the relative potency of species-specific forms of these hormones. Accordingly, we have examined the biological effects, interactions, and pharmacokinetics of equimolar doses (0.5 followed by 2.5 pmol.kg-1.min-1, each for 2 h) of species-specific forms of ANP, BNP-26, and CNP-22 in vehicle-controlled studies in normal conscious sheep. Although pharmacokinetics (metabolic clearance rates of 5.7 +/- 1.17, 7.5 +/- 1.36, and 4.7 +/- 0.71 l/min and half-lives of 3.9 +/- 0.42, 2.5 +/- 0.21, and 2.0 +/- 0.18 min for ANP, BNP, and CNP, respectively) are similar, the biological effects and actions on endogenous natriuretic peptide levels differ. Plasma BNP was significantly increased by CNP infusion (P < 0.0001), as was CNP by BNP infusions (P = 0.0009). Compared with ANP and BNP, which were equipotent in stimulating plasma guanosine 3',5'-cyclic monophosphate (cGMP; P < 0.0001 for both) and lowering arterial pressure (P < 0.05 for both) and cardiac output, CNP infusions induced only a small increment in cGMP and had no significant hemodynamic actions. In contrast, all three peptides suppressed plasma aldosterone levels (P < 0.05 for each), yet none induced significant natriuresis. Actions of CNP to increase BNP (and ANP) may account for the observed bioactivity of CNP. The findings show that potentially important interactions occur among all three hormones that need to be considered when interpreting the effects of individual peptides, particularly CNP.

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46

Vesely, David L. "Atrial Natriuretic Peptides." Journal of Investigative Medicine 53, no. 7 (November 2005): 360–65. http://dx.doi.org/10.2310/6650.2005.53708.

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Gehring, Chris, and Helen Irving. "Plant Natriuretic Peptides." Journal of Investigative Medicine 61, no. 5 (June 1, 2013): 823–26. http://dx.doi.org/10.2310/jim.0b013e3182923395.

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Farmakis, Dimitrios, John Parissis, George Papingiotis, John Lekakis, and Gerasimos Filippatos. "Natriuretic peptides revisited." Journal of Cardiovascular Medicine 17, no. 11 (November 2016): 840–42. http://dx.doi.org/10.2459/jcm.0000000000000447.

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Wang, Yu Hua, Lara Donaldson, Chris Gehring, and Helen R. Irving. "Plant natriuretic peptides." Plant Signaling & Behavior 6, no. 10 (October 2011): 1606–8. http://dx.doi.org/10.4161/psb.6.10.17304.

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Goetze, Jens P., Benoit G. Bruneau, Hugo R. Ramos, Tsuneo Ogawa, Mercedes Kuroski de Bold, and Adolfo J. de Bold. "Cardiac natriuretic peptides." Nature Reviews Cardiology 17, no. 11 (May 22, 2020): 698–717. http://dx.doi.org/10.1038/s41569-020-0381-0.

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Journal articles on the topic 'Natriuretic peptides'

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