RAAS

Renin-angiotensin Renin-angiotensin system

RAAS Schematic

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Anatomical diagram of RAAS.[1] The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood regulates blood pressure and pressure and water (fluid (fluid)) balance. hen blood !olume is low" the #idneys secrete renin renin.. Renin stimulates the production of angiotensin.. Angiotensin causes blood !essels to constrict resulting in increased blood pressure. angiotensin Angiotensin also stimulates the secretion of the hormone aldosterone from the adrenal corte$. corte$. Aldosterone causes the tubules of the #idneys to increase the reabsorption of sodium and water. This increases the !olume of fluid in the body" bo dy" which also increases blood pressure. %f the renin&angiotensin&aldosterone system is too acti!e" blood pressure will be too high. There are many drugs which interrupt different steps in this system to lower blood pressure. These drugs



The system can be acti!ated when there is a loss of blood of blood !olume !olume or a drop in blood in blood pressure (such as in hemorrhage hemorrhage). ). 1. %f the the perf perfus usio ion n of the the 'u$taglomerular apparatus in the #idney #idneys s macula densa decreases" densa decreases" then the 'u$taglomerular cells release the enyme renin renin.. *. Reni Renin n clea clea!e !ess a ymogen ymogen"" an inacti!e peptide inacti!e peptide"" called angiotensinogen angiotensinogen"" con!erting it into angiotensin I . +. Angiote Angiotensi nsin n % is is then then con!e con!erte rted d to angiotensin II by by angiotensin&con!erting enyme [] (A,-) which is found mainly in lung capillaries capillaries.. . Angiotensin Angiotensin %% is the the ma'or bioacti bioacti!e !e product of the renin&a renin&angiote ngiotensin nsin system" system" binding binding to receptors on intraglomerular mesangial cells" cells" causing these cells to contract along with the blood !essels surrounding them and causes cau ses the release of aldosterone of aldosterone from from the ona glomerulosa in the adrenal corte$. corte$. Angiotensin %% acts as an endocrine endocrine"" autocrine// paracrine" autocrine paracrine" and intracrine intracrine hormone. hormone. 0. atil 2aspal 2aspal et al. ha!e ha!e shown local local synthesis synthesis of Angiot Angiotensin ensin %%% %%% in neurons of sympat sympathetic hetic [0] ganglia.

Effects Further reading: Angiotensin#Effects reading: Angiotensin#Effects and Aldosterone#Function and Aldosterone#Function

%t is belie!ed that angiotensin % may ha!e some minor acti!ity" but angiotensin %% is the ma'or bio&acti!e product. Angiotensin Angiotensin %% has a !ariety of effects on the body3



pressure and decreasing the blood flow. 4owe!er" pressure and 4owe!er" the #idneys must continue to filter enough blood despite this drop in blood flow" necessitating necessitating mechanisms to #eep glomerular blood pressure up. To do this" angiotensin %% constricts efferent arterioles" which forces blood to build up in the glomerulus" increasing glomerular pressure. The glomerular filtration rate (56R) rate (56R) is thus maintained" and blood filtration can continue despite lowered o!erall #idney blood flow. 7ecause the filtration fraction has increased" there is less plasma fluid in the downstream peritubular capillaries. This in turn leads to a decreased hydrostatic pressure and increased osmotic pressure (due to u nfiltered plasma proteins) in the peritubular capillaries. The The effect of decreased hydrostatic pressure and increased osmotic pressure in the peritubular capillaries will facilitate increased reabsorption of tubular fluid. •

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Angiotensin %% decreases medullary blood flow through the !asa recta. This decreases the washout of 8a,l and urea in the #idney medullary space. Thus" higher concentrations o f 8a,l and urea in the medulla facilitate increased absorption of tubular fluid. 6urthermore" increased reabsorption of fluid into the medulla will increase passi!e reabsorption of sodium along the thin ascending limb of the loop of 4enle. Angiotensin %% stimulates 8a9/49 e$changers located on the apical membranes (faces the tubular lumen) of cells in the pro$imal tubule and thic# ascending limb of the loop of 4enle in addition to 8a9 channels in the collecting ducts. This will ultimately lead to increased sodium reabsorption Angiotensin %% stimulates the hypertrophy of renal tubule cells" leading to further sodium reabsorption. %n the adrenal corte$" corte$" it acts to cause the release of aldosterone aldosterone.. Aldosterone acts on the tubules (e.g the distal con!oluted tubules and tubules and the cortical collecting ducts) ducts) in the #idneys" causing them to reabsorb more sodium and water from the urine urine.. %n e$change for the reabsorbing of sodium to blood" potassium blood" potassium is secreted into the tubules" becomes part of urine and is e$creted. Aldosterone also acts on the central ner!ous system to increase an indi!iduals appetite for salt" and to stimulate the sensation of thirst thirst.. Release of anti&diuretic hormone (A:4)" also called !asopressin !asopressin && && A:4 is made in the hypothalamus and released from the posterior pituitary pituitary gland. gland. As its name suggests" it also e$hibits !aso&constricti!e properties" but its main course of action is to stimulate reabsorption of water in the #idneys.

These effects directly act in concert to increase blood pressure.

Clinical significance %nhibitors of angiotensin&con!erting enyme (A,enyme (A,- inhibitors) are often used to reduce



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:irect renin inhibitors are inhibitors are al alis# is#ire iren n[;] and the in!estigational rem remi# i#ire iren n[<]. As of 8o!ember *==>" a !accination !accination against against angiotensin %%" codenamed ,?T==;&Ang@b ,?T==;&Ang@b"" [>] is undergoing clinical trials.

Other uses of ACE %nterestingly" %nterestingly" A,- clea!es a number of other peptides" and in this capacity is an important regulator of the #inin&#alli#rein system. system.

Fetal renin-angiotensin system %n the fetus fetus"" the renin&angiotensin system is predominantly a sodium&losing system" as angiotensin %% has little or no effect on aldosterone le!els. Renin le!els are high in the fetus" while angiotensin %% le!els are significantly lower  this is due to the limited pulmonary blood flow" pre!enting pre!enting A,- (found predominantly in the pulmonary circulation) from ha!ing its ma$imum effect.

RAAS

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