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14-September-2008 18:02:45 - Atrial natriuretic peptide natriuretic peptide precursor A Identifiers Symbol NPPA Alt. Symbols ANP, PND Entrez 4878 HUGO 7939 OMIM 108780 RefSeq NM_006172 UniProt P01160 Other data Locus Chr. 1 p36.21 Atrial natriuretic peptide ANP, atrial natriuretic factor ANF, or atriopeptin, is a protein polypeptide hormone secreted by heart muscle cells. It is involved in the homeostatic control of body water, sodium, potassium and fat adiposity. It is released by muscle cells in the upper chambers atria of the heart atrial myocytes, in response to high blood pressure. ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure. Contents 1 Structure 2 Production 3 Receptors 4 Physiological effects 4.1 Renal 4.2 Vascular 4.3 Cardiac 4.4 Adipose tissue 5 Degradation 6 Other natriuretic factors 7 Diagnostic Use 8 Pharmacological modulation 9 See also 10 References 11 External links Structure ANP is a 28-amino acid peptide with a 17-amino acid ring in the middle of the molecule. The ring is formed by a disulfide bond between two cysteine residues at positions 7 and 23. ANP is closely related to BNP brain natriuretic peptide and CNP C-type natriuretic peptide, which all share the same amino acid ring. ANP was discovered in 1981 by a team in Kingston, Canada led by Adolfo J. de Bold after they made the seminal observation that injection of atrial but not ventricular tissue extracts into rats caused copious natriuresis.1 Production ANP is produced, stored and released by cardiac myocytes of the atria of the heart. It is released in response to atrial stretch and a variety of other signals induced by hypervolemia, exercise or caloric restriction. The hormone is constitutively expressed in the ventricle in response to stress induced by increased afterload eg. increased ventricular pressure from aortic stenosis or injury eg. myocardial infarction. ANP is secreted in response to: Atrial distention, stretching of the vessel walls Sympathetic stimulation of β-adrenoceptors Raised sodium concentration hypernatremia Angiotensin-II Endothelin, a potent vasoconstrictor The atria become distended by high extracellular fluid and blood volume, and atrial fibrillation. Notably, ANP secretion increases in response to immersion of the body in water, which causes atrial stretch due to an altered distribution of intravascular fluid. ANP secretion in response to exercise has also been demonstrated in horses. Receptors Three cell surface receptors have so far been identified on which ANP act, and these are designated ANPA, ANPB and ANPC. The ANPA and ANPB receptors have guanylate cyclase activity and mediate the biological effects by producing cGMP. The ANPC receptor functions mainly as a clearance receptor by binding and sequestering ANP from the circulation. All natriuretic peptides are bound by the ANPC receptor. Atrial natriuretic peptide and brain natriuretic peptide act through the ANPA and C-type natriuretic peptide through the ANPB receptor 2 Physiological effects ANP binds to a specific set of receptors - ANP receptors. Receptor-agonist binding causes a reduction in blood volume and therefore a reduction in cardiac output and systemic blood pressure. Lipolysis is increased and renal sodium reabsorption is decreased. The overall effect of ANP on the body is to counter increases in blood pressure and volume caused by the renin-angiotensin system. Renal Dilates the afferent glomerular arteriole, constricts the efferent glomerular arteriole, and relaxes the mesangial cells. This increases pressure in the glomerular capillaries, thus increasing the glomerular filtration rate GFR, resulting in greater excretion of sodium and water. Decreases sodium reabsorption in the distal convoluted tubule and cortical collecting duct of the nephron via guanosine 3',5'-cyclic monophosphate cGMP dependent phosphorylation of ENaC Inhibits renin secretion, thereby inhibiting the renin-angiotensin system. Reduces aldosterone secretion by the adrenal cortex. Vascular Relaxes vascular smooth muscle in arterioles and venules by: Membrane Receptor-mediated elevation of vascular smooth muscle cGMP Inhibition of the effects of catecholamines Cardiac Inhibits maladaptive cardiac hypertrophy Mice lacking cardiac NPRA develop increased cardiac mass and severe fibrosis and die suddenly Re-expression of NPRA rescues the phenotype. Adipose tissue Increases the release of free fatty acids from adipose tissue. Plasma concentrations of glycerol and nonesterified fatty acids are increased by i.v. infusion of ANP in humans. Activates adipocyte plasma membrane type A guanylyl cyclase receptors NPR-A Increases intracellular cGMP levels that induce the phosphorylation of a hormone-sensitive lipase and perilipin A via the activation of a cGMP dependent protein kinase-I cGK-I Does not modulate cAMP production or PKA activity Degradation Regulation of the effects of ANP is achieved through gradual degradation of the peptide by the enzyme neutral endopeptidase NEP. Recently NEP inhibitors have been developed, although they have not yet been licensed. They may be clinically useful in treating congestive heart disease. Other natriuretic factors In addition to the mammalian natriuretic peptides ANP, BNP, CNP, two others have been isolated. Tervonen 1998 described a salmon natriuretic peptide, named Salmon cardiac peptide, with similar structure and properties3. As well, dendroaspis natriuretic peptide DNP was discovered in the venom of the green mamba by Schweitz et al. 1992. Diagnostic Use Used in conjunction with other clinical information, measurement of B-type natriuretic peptide BNP can help determine whether a patient's dyspnea is caused by congestive heart failure in which BNP levels are elevated. This laboratory test has become a valuable and quick method for diagnostic work-up of patients presenting to the emergency department ED with acute dyspnea. Pharmacological modulation Neutral endopeptidase NEP is the enzyme that metabolizes natriuretic peptides. Several inhibitors of NEP are currently being developed to treat disorders ranging from hypertension to heart failure. Most of them are dual inhibitors. Omapatrilat dual inhibitor of NEP and angiotensin converting enzyme developed by BMS did not receive FDA approval due to angioedema safety concerns. Other dual inhibitors of NEP with ACE / angiotensin receptor are currently being developed by pharmaceutical companies.4 See also Brain natriuretic peptide Atrial volume receptors References ^ de Bold A 1985. Atrial natriuretic factor: a hormone produced by the heart. Science 230 4727: 767-70. doi:10.1126/science.2932797. PMID 2932797. ^ ANP ^ Tervonen et al., 1998 Endocrinology 139:4021-4025. ^ 1 Joshi Venugopal. 2003 Pharmacological modulation of the natriuretic peptide system. Expert Opinion on Therapeutic Patents 13:9, 1389 External links MeSH Atrial+Natriuretic+Factor v d e Endocrine system: hormones/endocrine glands Peptide hormones, Steroid hormones Hypothalamic-pituitary Hypothalamus: TRH, CRH , GnRH, GHRH, somatostatin, dopamine - Posterior pituitary: vasopressin, oxytocin - Anterior pituitary: α FSH, LH, TSH, GH, prolactin, POMC ACTH, MSH, endorphins, lipotropin Adrenal axis Adrenal medulla: epinephrine, norepinephrine - Adrenal cortex: aldosterone, cortisol, DHEA Thyroid axis Thyroid: thyroid hormone T3 and T4 - calcitonin - Parathyroid: PTH Gonadal axis Testis: testosterone, AMH, inhibin - Ovary: estradiol, progesterone, inhibin/activin, relaxin pregnancy Other end. glands Pancreas: glucagon, insulin, somatostatin - Pineal gland: melatonin Non-end. glands Placenta: hCG, HPL, estrogen, progesterone - Kidney: renin, EPO, calcitriol, prostaglandin - Heart atrium: ANP - Stomach: gastrin, ghrelin - Duodenum: CCK, GIP, secretin, motilin, VIP - Ileum: enteroglucagon - Adipose tissue: leptin, adiponectin, resistin - Thymus: Thymosin - Thymopoietin - Thymulin - Skeleton: Osteocalcin - Liver/other: Insulin-like growth factor IGF-1, IGF-2 Target-derived NGF, BDNF, NT-3 v d e Urinary system, physiology: renal physiology and acid base physiology Filtration Renal blood flow - Ultrafiltration - Countercurrent exchange Hormones affecting filtration Antidiuretic hormone ADH - Aldosterone - Atrial natriuretic peptide Secretion/clearance Pharmacokinetics - Clearance of medications Reabsorption Solvent drag - Na+ - Cl- - urea - glucose - oligopeptides - protein Endocrine Renin - Erythropoietin EPO - Calcitriol Active vitamin D - Prostaglandins Assessing Renal function/ Measures of dialysis Glomerular filtration rate - Creatinine clearance - Renal clearance ratio - Urea reduction ratio - Kt/V - Standardized Kt/V - Hemodialysis product - PAH clearance Effective renal plasma flow - Extraction ratio Acid base physiology Fluid balance - Darrow Yannet diagram - Body water - Interstitial fluid - Extracellular fluid - Intracellular fluid/Cytosol - Plasma - Transcellular fluid - Base excess - Davenport diagram - Anion gap - Arterial blood gas Buffering/compensation Bicarbonate buffering system - Respiratory compensation - Renal compensation Retrieved from http://en..org/wiki/Atrial_natriuretic_peptide Categories: Genes on chromosome 1 | Peptide hormones | Cardiac hormonesHidden category: Protein pages needing a picture Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch Þ‹Þ¨ÞˆÞ¬Þ€Þ¨Þ„Þ¦Þ?Þ° Español Français МакедонÑ?ки 日本語 Polski Português This page was last modified on 27 August 2008, at 23:42
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