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14-September-2008 18:02:41 - Angiotensin Redirected from Angiotensin II Angiotensinogen serpin peptidase inhibitor, clade A, member 8 Space-filling models of angiotensin I left and II right. From PDB 1N9U and 1N9V. Identifiers Symbols AGT; ANHU; SERPINA8 External IDs OMIM: 106150 MGI: 87963 HomoloGene: 14 Gene ontology Molecular function: serine-type endopeptidase inhibitor activity hormone activity type 1 angiotensin receptor binding type 2 angiotensin receptor binding Cellular component: extracellular region extracellular space soluble fraction Biological process: ovarian follicle rupture blood vessel development ureteric bud branching kidney development angiotensin mediated vasoconstriction during regulation of blood pressure renal response to blood flow during renin-angiotensin regulation of blood pressure renin-angiotensin regulation of aldosterone production angiotensin mediated regulation of renal output brain renin-angiotensin system cell-matrix adhesion cell surface receptor linked signal transduction cell-cell signaling female pregnancy establishment of blood-nerve barrier blood pressure regulation negative regulation of cell proliferation response to cold extracellular matrix organization and biogenesis peristalsis positive regulation of body size hormone metabolic process drinking behavior positive regulation of MAPKKK cascade negative regulation of neuron apoptosis positive regulation of fatty acid biosynthetic process positive regulation of organ size astrocyte activation smooth muscle cell proliferation smooth muscle cell differentiation RNA expression pattern More reference expression data Orthologs Human Mouse Entrez 183 11606 Ensembl ENSG00000135744 ENSMUSG00000031980 Uniprot P01019 Q3UTR7 Refseq NM_000029 mRNA NP_000020 protein NM_007428 mRNA NP_031454 protein Location Chr 1: 228.9 - 228.92 Mb Chr 8: 127.44 - 127.46 Mb Pubmed search 1 2 Angiotensin causes blood vessels to constrict, and drives blood pressure up. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also creates aldosterone, which causes the tubules of the kidneys to retain sodium and water, which also drives blood pressure up. Angiotensin is an oligopeptide in the blood that causes vasoconstriction, increased blood pressure, and release of aldosterone from the adrenal cortex. It is a hormone and a powerful dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. It plays an important role in the renin-angiotensin system. Angiotensin was independently isolated in Indianapolis and Argentina in the late 1930s as 'Angiotonin' and 'Hypertensin' respectively and subsequently characterised and synthesized by groups at the Cleveland Clinic and Ciba laboratories in Basel, Switzerland.1 Contents 1 Precursor, and types of angiotensin 1.1 Angiotensinogen 1.2 Angiotensin I 1.3 Angiotensin II 1.4 Angiotensin III 1.5 Angiotensin IV 2 Effects 2.1 Cardiovascular effects 2.2 Neural effects 2.3 Adrenal effects 2.4 Renal effects 3 See also 4 References 5 Further reading 6 External links Precursor, and types of angiotensin Angiotensinogen Angiotensinogen is an α-2-globulin that is produced constitutively and released into the circulation mainly by the liver. It is a member of the serpin family, although it is not known to inhibit other enzymes, unlike most serpins. Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels. Angiotensinogen is also known as renin substrate. Human angiotensinogen is 118 amino acids long, but other species have angiotensinogen of varying sizes2 Angiotensin I Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu Renin-angiotensin-aldosterone system Renin-angiotensin-aldosterone system Angiotensin I CAS# 11128-99-7 is formed by the action of renin on angiotensinogen. Renin is produced in the kidneys in response to both decreased intra-renal blood pressure at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa. If more Na+ is sensed, renin release is decreased. Renin cleaves the peptide bond between the leucine Leu and valine Val residues on angiotensinogen, creating the ten amino acid peptide des-Asp angiotensin I CAS# 9041-90-1. Angiotensin I appears to have no biological activity and exists solely as a precursor to angiotensin II. Angiotensin II Asp-Arg-Val-Tyr-Ile-His-Pro-Phe | His-Leu Angiotensin I is converted to angiotensin II through removal of two terminal residues by the enzyme Angiotensin-converting enzyme ACE, or kinase, which is found predominantly in the capillaries of the lung.3 ACE is actually found all over the body, but has its highest density in the lung due to the high density of capillary beds there. Angiotensin II acts as an endocrine, autocrine/ paracrine, and intracrine hormone. ACE is a target for inactivation by ACE inhibitor drugs, which decrease the rate of angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells which in turn activates contraction by an IP3-dependent mechanism. ACE inhibitor drugs are major drugs against hypertension. Other cleavage products of ACE, 7 or 9 amino acids long, are also known; they have differential affinity for angiotensin receptors, although their exact role is still unclear. The action of angiotensin II itself is targeted by angiotensin II receptor antagonists, which directly block angiotensin II AT1 receptors. Angiotensin II is degraded to angiotensin III by angiotensinases that are located in red blood cells and the vascular beds of most tissues. It has a half-life in circulation of around 30 seconds, while in tissue, it may be as long as 15-30 minutes. Angiotensin III Asp | Arg-Val-Tyr-Ile-His-Pro-Phe Angiotensin III has 40% of the pressor activity of Angiotensin II, but 100% of the aldosterone-producing activity. Angiotensin IV Arg | Val-Tyr-Ile-His-Pro-Phe Angiotensin IV is a hexapeptide which, like angiotensin III, has some lesser activity. Effects See also Renin-angiotensin_system#Effects Angiotensins II, III IV have a number of effects throughout the body: Cardiovascular effects It is a potent direct vasoconstrictor, constricting arteries and veins and increasing blood pressure. Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and production of PAI-1 and PAI-2.45 When cardiac cell growth is stimulated, a local autocrine-paracrine renin-angiotensin system is activated in the cardiac myocte, which stimulates cardiac cell growth through Protein Kinase C. The same system can be activated in smooth muscle cells in conditions of hypertension, atherosclerosis or endothelial damage. Angiotensin II is the most important Gq stimulator of the heart during hypertrophy, compared to endothelin-1 and A1 adrenoreceptors. Neural effects Angiotensin II increases thirst sensation dipsogen through the subfornical organ SFO of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers. Adrenal effects Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle. Renal effects Angiotensin II has a direct effect on the proximal tubules to increase Na+ absorption. It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting. Increases in systemic blood pressure will maintain renal perfusion pressure, however constriction of the afferent and efferent glomerular arterioles will tend to restrict renal blood flow. The effect on the efferent arteriolar resistance is, however, markedly greater, in part due to its smaller basal diameter; this tends to increase glomerular capillary hydrostat pressure and maintain glomerular filtration rate. A number of other mechanism can affect renal blood flow and GFR. High concentrations of Angiotensin II can constrict the glomerular mesangium reducing the area for glomerular filtration. Angiotensin II as a sensitizer to Tubuloglomerular feedback preventing an excessive rise in GFR. Angiotensin II causes the local release of prostaglandins which in turn antagonize renal vasoconstriction. The net effect of these completing mechanisms on glomerular filtration will vary with the physiological and pharmaclogical environment. Renal effects of Angiotensin II Target Action Mechanism6 Renal artery afferent arterioles vasoconstriction VDCCs -- Ca2+ influx efferent arteriole vasoconstriction probably activate Angiotensin receptor 1 -- Activation of Gq -- ↑PLC activity -- ↑IP3 and DAG -- activation of IP3 receptor in SR -- ↑intracellular Ca2+ mesangial cells contraction -- ↓filtration area activation of Gq -- ↑PLC activity -- ↑IP3 and DAG -- activation of IP3 receptor in SR -- ↑intracellular Ca2+ VDCCs -- Ca2+ influx Tubuloglomerular feedback Increased sensitivity Responsiveness increase of afferent arteriole to signals from macula densa medullary blood flow Reduction See also ACE inhibitor Angiotensin receptor Angiotensin II receptor antagonist References ^ Basso N, Terragno NA December 2001. History about the discovery of the renin-angiotensin system. Hypertension 38 6: 1246-9. PMID 11751697. ^ NCBI HomePage ^ Physiology at MCG 7/7ch09/7ch09p16 ^ Skurk T, Lee YM, Hauner H May 2001. Angiotensin II and its metabolites stimulate PAI-1 protein release from human adipocytes in primary culture. Hypertension 37 5: 1336-40. PMID 11358950. ^ Gesualdo L, Ranieri E, Monno R, et al August 1999. Angiotensin IV stimulates plasminogen activator inhibitor-1 expression in proximal tubular epithelial cells. Kidney Int. 56 2: 461-70. doi:10.1046/j.1523-1755.1999.00578.x. PMID 10432384. ^ Unless else specified in table, then ref is: Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 771 Further reading Brenner Rector's The Kidney, 7th ed., Saunders, 2004. Mosby's Medical Dictionary, 3rd Ed., CV Mosby Company, 1990. Review of Medical Physiology, 20th Ed., William F. Ganong, McGraw-Hill, 2001. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed., Burton David Rose Theodore W. Post McGraw-Hill, 2001 Lees KR, MacFadyen RJ, Doig JK, Reid JL 1993. Role of angiotensin in the extravascular system. Journal of human hypertension 7 Suppl 2: S7-12. PMID 8230088. Weir MR, Dzau VJ 2000. The renin-angiotensin-aldosterone system: a specific target for hypertension management. Am. J. Hypertens. 12 12 Pt 3: 205S-213S. PMID 10619573. Berry C, Touyz R, Dominiczak AF, et al. 2002. Angiotensin receptors: signaling, vascular pathophysiology, and interactions with ceramide. Am. J. Physiol. Heart Circ. Physiol. 281 6: H2337-65. PMID 11709400. Sernia C 2002. A critical appraisal of the intrinsic pancreatic angiotensin-generating system. JOP 2 1: 50-5. PMID 11862023. Varagic J, Frohlich ED 2003. Local cardiac renin-angiotensin system: hypertension and cardiac failure. J. Mol. Cell. Cardiol. 34 11: 1435-42. PMID 12431442. Wolf G 2006. Role of reactive oxygen species in angiotensin II-mediated renal growth, differentiation, and apoptosis. Antioxid. Redox Signal. 7 9-10: 1337-45. doi:10.1089/ars.2005.7.1337. PMID 16115039. Cazaubon S, Deshayes F, Couraud PO, Nahmias C 2006. Endothelin-1, angiotensin II and cancer. Med Sci Paris 22 4: 416-22. PMID 16597412. Ariza AC, Bobadilla NA, Halhali A 2007. Endothelin 1 and angiotensin II in preeeclampsia. Rev. Invest. Clin. 59 1: 48-56. PMID 17569300. External links MeSH Angiotensins v d e Cardiovascular system, physiology: cardiovascular physiology Volumes Preload - Afterload - End-systolic volume - End-diastolic volume - Frank-Starling law of the heart Interactions Cardiac output - Cardiac cycle - Wiggers diagram - Pressure volume diagram Tropism Chronotropic - Dromotropic - Inotropic - Batmotropic - Lusitropic Hemodynamics Baroreflex - Kinin-kallikrein system - Renin-angiotensin system - Vasoconstrictors - Vasodilators - Compliance - Vascular resistance Other Electrical conduction system of the heart Cardiac action potential - Heart sounds Gallop rhythm, Third heart sound, Fourth heart sound - Pulse - Blood flow v d e Peptides: neuropeptides Hypothalamic Somatostatin - CRH - GnRH - GHRH - Orexins - TRH - POMC ACTH, MSH, Lipotropin Gastrointestinal hormones Cholecystokinin - Gastric inhibitory polypeptide - Gastrin - Motilin - Secretin - Vasoactive intestinal peptide Other hormones Vasopressin - Calcitonin - Other Angiotensin - Bombesin/Neuromedin B - Calcitonin gene-related peptide - Carnosine - Delta sleep-inducing peptide - FMRFamide - Galanin - Gastrin releasing peptide - Kinins Bradykinin, Tachykinins - Neuromedin B, N, U - Neuropeptide Y - Neurophysins - Neurotensin - Opioid peptide - Pancreatic polypeptide - Pituitary adenylate cyclase activating peptide v d e Autacoids Angiotensin - Eicosanoid - Histamine - Kinin - Platelet-activating factor - Serotonin Retrieved from http://en..org/wiki/Angiotensin Categories: Genes on chromosome 1 | Human proteins | Peptide hormones | Cardiovascular system | Endocrinology | Physiology 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 Nederlands 日本語 Polski Português РуÑ?Ñ?кий СрпÑ?ки / Srpski Suomi Svenska This page was last modified on 29 August 2008, at 17:40
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