angiotensin
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an·gi·o·ten·sin
Oxford Dictionary of Sports Science & Medicine:
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angiotensin
A protein that has two forms: angiotensin I and angiotensin II. Angiotensin I is derived from a plasma protein and released by the action of renin from the kidneys. The function of angiotensin I is unclear. However, it forms angiotensin II when acted on by an enzyme called angiotensin converting enzyme (ACE). Angiotensin II has two amino acid units less than angiotensin I. It increases the output of aldosterone from the adrenal cortex. Angiotension II can also cause blood vessels to constrict thus raising blood pressure. It can also indirectly raise blood pressure and blood volume by stimulating the thirst centres in the brain and directing the kidney to conserve more water and minerals. See also angiotensin-converting enzyme.
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Hypertensin
IN BRIEF: n. any of several vasoconstrictor pressor polypeptides, also called angiotonin
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Oxford Dictionary of Biochemistry:
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angiotensin
any of three related peptides, two of which regulate adrenal activity and also increase vasoconstriction and raise blood pressure. Angiotensin I, the decapeptide H — Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu — OH, is cleaved off angiotensinogen by the kidney enzyme renin; this peptide has no physiologically important action. Angiotensin II, the octapeptide formed from angiotensin I by removal of -His-Leu — OH by the action of angiotensin converting enzyme, is the most powerful pressor agent known, and the substance responsible for essential hypertension. It is also one of the most potent known stimulators of aldosterone production by the adrenal gland. It is rapidly destroyed by tissue peptidases, including angiotensinase. Angiotensin III, the heptapeptide formed by removal of the N-terminal Asp residue from angiotensin II (and the only one of its breakdown products to have activity), appears to be as active on the adrenal gland as angiotensin II, and may also have significant vasoconstrictor activity.
| angiostatin, angiosperm, angiopoietin | |
| angiotensin converting enzyme, angiotensin converting enzyme inhibitors, angiotensin receptor |
Saunders Veterinary Dictionary:
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angiotensin
A vasoconstrictive principle formed in the blood when renin is released from the juxtaglomerular apparatus in the kidney. The enzymatic action of renin cleaves a serum α2-globulin, angiotensinogen, forming the decapeptide angiotensin I, which is relatively inactive. It in turn is acted upon by peptidases (converting enzymes), chiefly in the lungs, to form the octapeptide angiotensin II, a powerful vasopressor and a stimulator of aldosterone secretion by the adrenal cortex. By its vasopressor action, it raises blood pressure and diminishes fluid loss in the kidney by restricting blood flow. Angiotensin II is hydrolyzed in various tissues to form heptapeptide angiotensin III, which has less vasopressor activity but more effect on the adrenal cortex.
- a. amide — an amide derivative of angiotensin II which is a powerful vasoconstrictor and vasopressor, and is used in the treatment of certain hypotensive states; usually administered by slow intravenous infusion, and sometimes intramuscularly or subcutaneously.
- a.-converting enzyme (ACE) — a peptidase which catalyzes the formation of angiotensin II from angiotensin I. See also ace.
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Angiotensin
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This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (March 2012) |
Angiotensin is a peptide hormone that causes vasoconstriction and a subsequent increase in blood pressure. It is part of the renin-angiotensin system, which is a major target for drugs that lower blood pressure. Angiotensin also stimulates the release of aldosterone, another hormone, from the adrenal cortex. Aldosterone promotes sodium retention in the distal nephron, in the kidney, which also drives blood pressure up.
Angiotensin is an oligopeptide and 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]
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Contents
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Precursor, and types of angiotensin
Angiotensinogen
Angiotensinogen is an α-2-globulin 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 452 amino acids long, but other species have angiotensinogen of varying sizes. The first 12 amino acids are the most important for activity.
Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile-...
Angiotensin I
Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu | Val-Ile-...
Angiotensin I (CAS# 11128-99-7) is formed by the action of renin on angiotensinogen. Renin is produced in the kidneys in response to renal sympaticus activity, decreased intrarenal blood pressure (<90mmHg systolic blood pressure[2] ) at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa.[3] If less Na+ is sensed by the macula densa, renin release by juxtaglomerular cells is increased.
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 2.
Angiotensin II
Asp-Arg-Val-Tyr-Ile-His-Pro-Phe | His-Leu
Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE, or kinase), primarily through ACE within the kidney. ACE found in other tissues of the body has no physiological role (ACE has a high density in the lung, but activation here promotes no vasoconstriction, angiotensin II is below physiological levels of action). 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 AII 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, seven 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 AII itself is targeted by angiotensin II receptor antagonists, which directly block angiotensin II AT1 receptors.
Angiotensin II is degraded to angiotensin III by angiotensinases located in red blood cells and the vascular beds of most tissues. It has a half-life in circulation of around 30 seconds, whereas, 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 that, like angiotensin III, has some lesser activity.
Effects
- See also Renin-angiotensin_system#Effects
Angiotensins II, III and IV have a number of effects throughout the body:
Cardiovascular
They are potent direct vasoconstrictors, 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.[4][5]
When cardiac cell growth is stimulated, a local (autocrine-paracrine) renin-angiotensin system is activated in the cardiac myocyte, 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 α1 adrenoreceptors.[citation needed]
Neural
Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ 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
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
Angiotensin II has a direct effect on the proximal tubules to increase Na+ reabsorption. 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 hydrostatic pressure and maintain glomerular filtration rate. A number of other mechanisms 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 competing mechanisms on glomerular filtration will vary with the physiological and pharmacological environment.
| Target | Action | Mechanism[6] |
|---|---|---|
| renal artery & afferent arterioles |
vasoconstriction (weaker) | VDCCs → Ca2+ influx |
| efferent arteriole | vasoconstriction (stronger) | (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 | |
| proximal tubule | increased Na+ reabsorption |
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| tubuloglomerular feedback | increased sensitivity | increase in afferent arteriole responsiveness to signals from macula densa |
| medullary blood flow | reduction |
See also
- ACE inhibitor
- Angiotensin receptor
- Angiotensin II receptor antagonist
- Captopril
- Peptides
- Renin inhibitor
References
- ^ Basso N, Terragno NA (December 2001). "History about the discovery of the renin-angiotensin system". Hypertension 38 (6): 1246–9. doi:10.1161/hy1201.101214. PMID 11751697.
- ^ "JAMA Article Jan 2012". http://jama.ama-assn.org/content/280/13/1168.full.
- ^ Williams GH, Dluhy RG (2008). "Chapter 336: Disorders of the Adrenal Cortex". In Loscalzo J, Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL. Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-146633-9.
- ^ 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. http://hyper.ahajournals.org/cgi/pmidlookup?view=long&pmid=11358950.
- ^ Gesualdo L, Ranieri E, Monno R et al (August 1999). "Angiotensin IV stes 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.
- ^ Boulpaep EL, Boron WF (2005). Medical Physiology: a Cellular and Molecular Approach. St. Louis, Mo: Elsevier Saunders. pp. 771. ISBN 1-4160-2328-3.
Further reading
- de Gasparo M, Catt KJ, Inagami T, "" et al (2000). "International union of pharmacology. XXIII. The angiotensin II receptors". Parmacol Rev. 52 (3): 415–472. PMID 10977869.
- 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. doi:10.1016/S0895-7061(99)00103-X. 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. doi:10.1006/jmcc.2002.2075. 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. doi:10.1051/medsci/2006224416. 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
- The MEROPS online database for peptidases and their inhibitors: I04.953
- MeSH Angiotensins
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