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07-SEPTEMBER-2008 03:17:44 - Renin-angiotensin system Redirected from Renin-angiotensin RAAS Schematic RAAS Schematic The renin-angiotensin system RAS or the renin-angiotensin-aldosterone system RAAS is a hormone system that regulates blood pressure and water fluid balance. When blood pressure is low, the kidneys secrete renin. Renin stimulates the production of angiotensin. Angiotensin causes blood vessels to constrict resulting in increased blood pressure. Angiotensin also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to retain sodium and water. This increases the volume of fluid in the body, which also increases blood pressure. If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. There are many drugs which interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure hypertension, heart failure, kidney failure, and harmful effects of diabetes.12 Contents 1 Activation 2 Effects 3 Clinical significance 4 Other uses of ACE 5 Fetal renin-angiotensin system 6 References 7 External links Activation The system can be activated when there is a loss of blood volume or a drop in blood pressure such as in hemorrhage. If the perfusion of the juxtaglomerular apparatus in the kidneys decreases, then the juxtaglomerular cells release the enzyme renin. Renin cleaves an inactive peptide called angiotensinogen, converting it into angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme ACE3 which is found mainly in lung capillaries. Angiotensin II is the major bioactive product of the renin-angiotensin system. Angiotensin II acts as an endocrine, autocrine/ paracrine, and intracrine hormone. Patil Jaspal et. al. has shown local synthesis of Angiotensin II in neurons of sympathetic ganglia.4 Effects Further reading: Angiotensin#Effects and Aldosterone#Function It is believe that Angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin II has a variety of effects on the body: Throughout the body, it is a potent vasoconstrictor of arterioles. In the kidneys, it constricts glomerular arterioles, having a greater effect on efferent arterioles than afferent. As with most other capillary beds in the body, the constriction of afferent arterioles increases the arteriolar resistance, raising systemic arterial blood pressure and decreasing the blood flow. However, the kidneys must continue to filter enough blood despite this drop in blood flow, necessitating mechanisms to keep glomerular blood pressure up. To do this, Angiotensin II constricts efferent arterioles, which forces blood to build up in the glomerulus, increasing glomerular pressure. The glomerular filtration rate GFR is thus maintained, and blood filtration can continue despite lowered overall kidney blood flow. In the adrenal cortex, it acts to cause the release of aldosterone. Aldosterone acts on the tubules e.g the distal convoluted tubules and the cortical collecting ducts in the kidneys, causing them to reabsorb more sodium and water from the urine. Potassium is secreted into the tubules in exchange for the sodium, which is excreted. Aldosterone also acts on the central nervous system to increase an individual's appetite for salt, and to stimulate the sensation of thirst. Release of Anti-Diuretic Hormone ADH, also called vasopressin -- ADH is made in the hypothalamus and released from the posterior pituitary gland. As its name suggests, it also exhibits vaso-constrictive properties, but its main course of action is to stimulate reabsorption of water in the kidneys. These effects directly act in concert to increase blood pressure. Clinical significance The renin-angiotensin system is often manipulated clinically to treat high blood pressure. Inhibitors of angiotensin-converting enzyme ACE inhibitors are often used to reduce the formation of the more potent angiotensin II. Captopril is an example of an ACE inhibitor. Alternatively, angiotensin receptor blockers ARBs can be used to prevent angiotensin II from acting on angiotensin receptors. A new drug called Aliskiren released in 2007 acts by directly inhibiting renin receptors. Other uses of ACE Interestingly, ACE cleaves a number of other peptides, and in this capacity is an important regulator of the kinin-kallikrein system. Fetal renin-angiotensin system In the fetus, the renin-angiotensin system is predominantly a sodium-losing system, as angiotensin II has little or no effect on aldosterone levels. Renin levels are high in the fetus, while angiotensin II levels are significantly lower - this is due to the limited pulmonary blood flow, preventing ACE found predominantly in the pulmonary circulation from having its maximum effect. References ^ High Blood Pressure: Heart and Blood Vessel Disorders. Merck Manual Home ion. ^ Solomon, Scott D; Anavekar, Nagesh 2005. A Brief Overview of Inhibition of the Renin-Angiotensin System: Emphasis on Blockade of the Angiotensin II Type-1 Receptor. Medscape Cardiology 9 2. ^ Paul M, Poyan Mehr A, Kreutz R July 2006. Physiology of local renin-angiotensin systems. Physiol. Rev. 86 3: 747-803. doi:10.1152/physrev.00036.2005. PMID 16816138. ^ Patil J, Heiniger E, Schaffner T, Mühlemann O, Imboden H April 2008. Angiotensinergic neurons in sympathetic coeliac ganglia innervating rat and human mesenteric resistance blood vessels. Regul. Pept. 147 1-3: 82-7. doi:10.1016/j.regpep.2008.01.006. PMID 18308407. Banic A, Sigurdsson GH, Wheatley AM 1993. Influence of age on the cardiovascular response during graded haemorrhage in anaesthetized rats. Res Exp Med Berl 193 5: 315-21. PMID 8278677. External links MeSH Renin-Angiotensin+System 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 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/Renin-angiotensin_system Categories: Cardiovascular system | Endocrinology 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 Dansk Deutsch Français Italiano עברית Nederlands 日本語 ‪Norsk bokmÃ¥l‬ Polski Português РуÑ?Ñ?кий SlovenÄ?ina Svenska This page was last modified on 3 August 2008, at 23:15
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