Natriuretic peptide

Natriuretic peptides (ANP, BNP, CNP) were first described by Genest and are now recognized to have several autocrine and paracrine effects within the myocardium and coronary circulation. Natriuretic peptide receptor A (NPR-A) and B (NPR- B) are widely expressed in the cardiovascular system. The natriuretic peptides produce cellular responses through the elevation of intracellular c-GMP concentration that in turn regulates 

PKG and cyclic nucleotide phosphodiesterases (PDEs) (reviewed by Baxter37). A rapid release of natriuretic peptides and induction of their de novo synthesis occurs in myocardial ischemia. Natriuretic peptides may have a cardioprotective role. BNP-32 administration in perfused rat hearts prior to left main coronary artery occlusion and until 30 min of reperfusion resulted in limitation of infarct size in a concentration dependent manner. Furthermore, this effect was abolished by 5-hydroxydecanoate (presumed to be a selective blocker of mitochondrial KATp channels), L-NAME, an inhibitor of NOS and ODQ, a specific soluble guanyl cyclase inhibitor.38 Similarly, human recombinant ANP limited infarct size and reperfusion arrhythmias in a canine model of coronary occlusion and reperfusion.39 

PTHrP is structurally related to parathyroid hormone (PTH). In contrast to PTH, which is exclusively expressed in and secreted by the parathyroid gland, PTHrP is expressed and released by vascular smooth muscle cells and endothelial cells but not by ventricular myocytes. PTH and PTHrP are potent dilators and exert positive chronotropic and inotropic effects (reviewed by Halapas40). PTHrP activates adenyl cyclase and increases c-AMP levels with subsequent activation of PKA/PKC dependent pathways.41,42 

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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. 

ANPs play an important role in the maintenance of cardiovascular homeostasis by counterbalancing the renin—angiotensin (RAS) system. ANP, the main circulating form of the natriuretic peptides, effectively relaxes vascular smooth muscle, promotes the excretion of sodium and water, and in the CNS inhibits vasopressin release and antagonizes AT-II induced thirst. 

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 ... 

Urodilantin, a 32-amino acid natriuretic peptide synthesized by the kidney and found in urine but not in plasma, is beheved to compHcate the interpretation of the natriuretic effects of ANP (58). There have been reports of natriuretic peptides related to ANP that have been isolated from several sources, including the brain, eg, brain natriuretic peptide (BNP) [114471-18-0] (59—61). 

Human brain natriuretic peptide (BNP) is a small peptide of 32 amino acids used in the treatment of congestive heat failure. How many nitrogen bases are present in the DNA that codes for BNP ... 

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... 

Because renal vasodilatation and hyperfiltration are often associated with a natriuretic response, a number of activators or inhibitors of endogenous vasoactive systems can cause increased NaCl excretion, and some of these may be developed into compounds of clinical interest in special situations. Such agents include natriuretic pqDtides most notably B-type natriuretic peptide (nesiritide), neutral endopeptidase (NEP) inhibitors (thiorphan, phosphoramidon), mixed NEP and ACE inhibitors (omapatrilat), guanylin and uroguanylin, kinins, prostaglandins of the E series, adrenomedullin, relaxin, prolactin, and others. 

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... 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

BNP, B-type natriuretic peptide BP, blood pressure ECC, electrocardiogram HR, heart rate. 

A-Z Health Guide from WebMD. Medical Tests Brain Natriuretic Peptide (BNP) Test. Available at www.webmd.com/hw/ heart disease/uxl072.asp accessed November 21, 2005. 

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. 

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