Atrial natriuretic peptide mechanism

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 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) 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 ... 

The expression of the ET-1 gene is increased by growth factors and cytokines, including transforming growth factor-B (TGF-B) and interleukin 1 (IL-1), vasoactive substances including angiotensin II and vasopressin, and mechanical stress. Expression is inhibited by nitric oxide, prostacyclin, and atrial natriuretic peptide. 

An additional mechanism controlling lipolysis specifically in humans has recently come to light (J. Galitsky, 2000). Atrial natriuretic peptide has a potent stimulatory effect on lipolysis in human adipocytes, where administration of the peptide was associated with increased phosphorylation of HSL and perilipin. This effect was blocked by inhibition of cGMP-dependent protein kinase I. At this point it is unclear whether this kinase phospho-rylates HSL and perilipin directly or if it has an indirect effect mediated through PKA. 

Diuretics are drugs that increase the rate of urine flow clinically useful diuretics also increase the rate of excretion of Na+ (natiiuresis) and an accompanying anion, usually CD. Most clinical applications of diuretics aim to reduce extracellular fluid volume by decreasing total-body NaCl content. Although continued administration of a diuretic causes a sustained net deficit in total-body Na+, the time course of natriuresis is finite because renal compensatory mechanisms bring Na+ excretion in line with Na+ intake, a phenomenon known as diuretic braking. Compensatory mechanisms include activation of the sympathetic nervous system, activation of the renin-angiotensin-aldosterone axis, decreased arterial blood pressure (which reduces pressure natriuresis), hypertrophy of renal epithelial cells, increased expression of renal epithelial transporters, and perhaps alterations in natriuretic hormones such as atrial natriuretic peptide. 

Scott-Woo GC, Sutherland C, Walsh MP (1990) Kinase activity associated with caldes-mon is Ca /calmodulin-dependent kinase II. Biochem J 268 367-370 Seguchi H, Nishimura J, Toyofuku K, Kobayashi S, Kumazawa J, Kanaide H (1996) The mechanism of relaxation induced by atrial natriuretic peptide in the porcine renal artery. British J Pharmacol 118 343-351... 

An additional mechanism for regulating sodium reabsorption is the atrial natriuretic peptide (ANP) mechanism ... 

Wang W-J, He L, Chen J, Dinger B, Fidone S. Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body. J Physiol 1993 460 427-441. 

He L, Dinger B, Fidone S. Cellular mechanisms involved in carotid body inhibition produced by atrial natriuretic peptide. Am J Physiol Cell Physiol 2000 278 C845-C852. 

Miscellaneous Agents - Atriopeptins I and II (Atl and Atll), two peptides of atrial tissue origin, have been isolated and characterized. These substances are diuretic, natriuretic and relax intestinal (Atl and Atll) and vascular (Atll) tissue.The discovery of these compounds suggests a new endogenous control mechanism involving the heart and kidneys that may be important for maintenance of normal blood pressure. 

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