Atrial natriuretic peptides

Atrial Natriuretic Peptide, a-Atrial natriuretic peptide [85637-73-6] (ANP) (55), also known as atrial natriuretic factor (ANF), brain natriuretic peptide (BNP) (56), and type C natriuretic peptide (CNP) (57) are members of the ANP family (28). These atrial peptides arise from a common 128 amino acid precursor where the active form of ANP is the 28 amino acid peptide at the C terminus. 

Natriuretic Peptide Diuretics. Atrial natriuretic peptide (ANP), an endogenous diuretic, natriuretic, and vasodilator, is a peptide hormone primarily synthesized and stored by atrial cardiocytes, and secreted by the atria in response to mechanical stretch of the atria. It was discovered in the cmde extracts of atria in 1981 (51). ANP is also known as anaritide [95896-08-5] atrial natriuretic factor [104595-79-1] (ANF) auriculin ... 

The atrial natriuretic peptide (ANP) belongs to a family of hormones that have structural similarity and some biological actions in common, such as natriuresis and haemoconcentration. It is synthesized and secreted by the cardiac atrium in response to increased atrial pressure. ANP is believed to act physiologically in an opposing manner to AVP... 

Endothelial cells are the major source of ET-1-synthesis. ET-1 is also produced by astrocytes, neurons, hepatocytes, bronchial epithelial cells, renal epithelial and mesangial cells. Physiological stimuli of ET-1-synthesis in endothelial cells are angiotensin II, catecholamines, thrombin, growth factors, insulin, hypoxia and shear stress. Inhibitors of ET-1 synthesis are atrial natriuretic peptide, prostaglandin E2 and prostacyclin. ET-2 is mainly synthesized in kidney, intestine, myocardium and placenta and ET-3 is predominantely produced by neurons, astrocytes and renal epithelial cells. 

Natriuretic peptides are a family of peptide hormones. All of them contain a 17-amino acid long ring that is closed by a disulfide bond between two cysteine residues. ANP (atrial natriuretic peptide) is mainly expressed in the atria of the heart, whereas BNP (B-type natriuretic peptide) is synthesized in the ventricular myocardium. CNP occurs mainly in the endothelium and is thought to have a paracrine function. ANF and BNF lower blood pressure by a direct effect on smooth muscle and on the salt retention in the kidney. Natriuretic peptides bind and activate particulate guanylyl cyclases. 

Urodilatin is a peptide similar to atrial natriuretic peptide, which is produced in the distal tubule of the kidney and promotes sodium excretion and diuresis by acting on receptors localized on the luminal site of the collecting duct of the nephron. 

ANAb Anti-nuclear antibodies ANCA Anti-neutrophil cytoplasmic auto antibodies cANCA Cytoplasmic ANCA pANCA Perinuclear ANCA AND Anaphylactic degranulation ANF Atrial natriuretic factor ANP Atrial natriuretic peptide Anti-I-A, Anti-I-E Antibody against class II MHC molecule encoded by I-A locus, I-E locus, anti-lg Antibody against an immunoglobulin... 

Atrial natriuretic peptide A type of peptide, 28 amino acids in length, secreted by the atria of the heart when atrial pressure and stretch are increased. 

Nussberger, J., Mooser, V., Maridor, G., Juillerat, L., Waeber, B. and Brunner, H., Caffeine-induced diuresis and atrial natriuretic peptides. J Cadiovasc Pharmacol 15(5), 685-691, 1990. 

Substances released by the heart as atrial natriuretic peptide (ANP) have also offered a new dimension when looking at regulators of circulation (see Sect. 5.2.3) (Y2). 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

B8. Beishuizen, A, Gotz, J. M., Kip, L Haanen, C., and Vermes, I Elevated plasma levels of endothelin are associated with the severity of sepsis and presence of shock in contrast to the levels of atrial natriuretic peptide. Med. Inflam. 1,419-423 (1992). 

F21. Fukuda, Y., Hirata, Y., Yoshimi, H., Kojima, T., Kobayashi, Y Yanagisawa, M and Masaki, T., Endothelin is a potent secretagogue for atrial natriuretic peptide in cultured rat atrial myocytes. Biochem. Biophys. Res. Commun. 155,167-172 (1988). 

H24. Hinder, F Booke, M Traber, L. D., Matsumoto, N., Nishida, K Rogers, S and Traber, D. L., Nitric oxide synthase inhibition during experimental sepsis improves renal excretory function in the presence of chronically increased atrial natriuretic peptide. Crit. Care Med. 24,131 -136 (1996). 

M30. Mitaka, C., Nagura, T., Sakanishi, N Tsunoda, Y., and Toyooka, H., Plasma a-atrial natriuretic peptide concentrations in acute respiratory failure associated with sepsis Preliminary study. Crit. Care Med. 18, 1201-1203 (1990). 

Rl. Raff, H., and Findling, J. W., Aldosterone control in critically ill patients ACTH, metoclo-propamide, and atrial natriuretic peptide. Crit. Care Med. 18,915-920 (1990). 

Stasch, J. P., Hirth-Dietrich, C., Kazda, S., and Neuser, D., Endothelin stimulates release of atrial natriuretic peptides in vitro and in vivo. Life Sci. 45,869-875 (1989). 

Indicate the source, factors regulating the release, and physiological significance of the following vasodilators prostacyclin, nitric oxide, and atrial natriuretic peptide... 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

Atrial natriuretic peptide (ANP) is produced by specialized myocytes in the atria of the heart. Secretion is stimulated by increased filling and stretch of the atria in response to plasma volume expansion. The effects of ANP include vasodilation, diuresis (increased urine production), and increased sodium excretion. Taken together, these effects decrease blood volume and blood pressure toward normal. 

Atrial natriuretic peptide (ANP) released from myocardial cells in the atria of the heart inhibits the reabsorption of sodium from the collecting duct. The mechanisms of action of ANP include ... 

Atrial natriuretic peptide is released from myocardial cells in the atria of the heart in response to an increase in atrial filling, or an increase in plasma volume. This hormone inhibits the release of renin. With less angiotensin Il-induced vasoconstriction of the afferent arteriole, RBF, GFR, and urine output increase. The increased loss of water and solutes decreases blood volume toward normal. 

Sodium reabsorption is also influenced by ANP. The original decrease in plasma volume leads to a decrease in atrial filling and a decrease in the release of ANP from the myocardium. Atrial natriuretic peptide, which acts on vascular smooth muscle, granular cells of the kidney, and the adrenal cortex, normally causes the following ... 

TBTC1 produced a dose-dependent inhibition of ANP on vascular smooth muscle responses with an effect on norepinephrine, nitroprusside and atrial natriuretic peptide in isolated aortic rings of rats. The inhibition of vasorelaxation was accompanied by a parallel inhibition of ANP-induced cGMP generation29. 

ANF atrial natriuretic peptide CGRP calcitonin gene-related peptide VIP vasoactive intestinal peptide... 

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