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Hormones atrial natriuretic peptide

The endogenous hormone atrial natriuretic peptide (ANP), which acts to increase blood pressure, is, like many other effector peptides, excised from a longer native chain by an endopeptidase enzyme, that is, an agent that cleaves bonds well along the chain of amino acids. A small-molecule endopeptidase inhibitor lowers blood pressure by inhibiting the release of ANP. The inhibitor candoxatril (6-8) is now... [Pg.92]

Space travel is associated with a decrease in blood and plasma volumes and is further associated with increases in plasma antidiuretic hormone, atrial natriuretic peptide, growth hormone, cortisol, and corticotropin concentrations. In contrast, the plasma renin activity may be decreased by as much as 50%. Plasma aldosterone may also decrease but to a lesser extent. In spite of the stress of space travel the plasma concentrations of catecholamines are usually unaffected. Plasma and urine calcium concentrations increase during... [Pg.453]

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 ... [Pg.208]

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... [Pg.237]

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. [Pg.820]

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). [Pg.99]

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. [Pg.334]

The steroid hormone aldosterone (see p. 55) increases Na reuptake, particularly in the distal tubule, while atrial natriuretic peptide (ANP) originating from the cardiac atrium reduces it. Among other effects, aldosterone induces Na /K" ATPase and various Na" transporters on the luminal side of the cells. [Pg.328]

Contractile elements of the podocyte foot processes, which may influence the hydraulic permeability of the glomerular capillary wall, may be regulated via vasoactive hormones. Receptors for some vasoactive hormones, for example, en-dothelin (R4), atrial natriuretic peptide (S9), nitric oxide (K22), and angiotensin n (Yl), have been described on the podocyte surface. [Pg.179]

Atrial natriuretic peptides (ANP) a hormone that is released by cardiac cells following a high blood pressure. It is involved in the control of water, sodium and adiposity. It is also known as atrial natriuretic factor (ANF) and atriopeptin. [Pg.321]

Interaction with phospholipid bilayers of a number of hormones, such as atriopeptin HI, an atrial natriuretic peptide, and of calcitonin was investigated by Surewicz et al. [Pg.370]

ATRIOPEPTIN-28 (HUMAN) CARPERITIDE HORSE ATRIAL NATRIURETIC PEPTIDE-28 HUMAN ATRIAL NATRIURETIC FACTOR (99-126) a-hmn ATRIAL NATRIURETIC HORMONE HUMAN ATRIAL NATRIURETIC PEPTIDE (1-28) (99-126) HUMAN ATRIOPEPTIN(l-28) HUMAN ATRIOPEPTIN(99-126) (99-126)-hmn PROATRIOPEPTIN SUN-4936 TRIO-PEPTIN (HUMAN a-COMPONENT)... [Pg.731]

The earliest endocrine abnormality in almost all types of cardiac disease is increased release of the heart s own hormones, the natriuretic peptides ANP and BNP (A for atrial, B for brain, where it was first discovered), and their concentration in plasma may become a guide to therapy. These peptides normally suppress renin and aldosterone production. [Pg.514]

Lavendustin A and derivatives have been used to study the pathophysiological role of protein kinases. For instance, lavendustin A was used to study the potential role of tyrosine kinases in the regulation of wall stretch-induced atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) secretion. Because lavendustin A is selective for t5n-osine kinases, the data obtained under these conditions showed that this kind of kinase is implicated in regulating cardiac hormone secretion. However, it is still unclear which tyrosine kinase is responsible for wall stretch-induced cardiac hormone secretion [111]. [Pg.870]

ATRIAL NATRIURETIC PEPTIDE RECEPTOR AGONISTS include ANP itself (also called atrial natriuretic factor (ANF), or atrlopeptin), a peptide made up of 28 amino acids and is contained in secretory granules in heart atrial cells. ANP is released in response to stretch in the atria, as occurs with increased central venous pressure, thus signalling volume overload in the circulation. The peptide has an effect on the kidney leading to increased Na and water excretion, vasodilation, increased vascular permeability and modified release of a number of other hormones and neurotransmitters. There are at least three related endogenous peptides ANP (atrial natriuretic peptide),... [Pg.42]

Atrial natriuretic peptide has a beneficial local hormone effect on the heart, and, theoretically, agents that mimic or enhance its effects may be useful in heart failure, e.g. candoxatril. [Pg.42]

Renal epithefial cell membranes also contain proteins that act as ion channels. For example, there is one for sodium that is closed by amiloride and modulated by hormones such as atrial natriuretic peptide (ANP). Ion channels enable much... [Pg.1678]


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See also in sourсe #XX -- [ Pg.720 ]




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Atrial natriuretic peptide

Natriuretic hormone

Natriuretic peptides

Peptide hormones

Peptidic hormones

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