Renin-angiotensin-aldosterone system

Features and funtions of the components of RAAS

 renal  endocrinology  hypertension

angiotensinogenangiotensin Iangiotensin IIaldosterone
locationproduced in the liver and released into the circulationformed in the kidneyformed mainly in lungs and kidneyproduced in adrenal cortex
productionincreased production in response to corticosteroids, oestrogen and thyroxinefrom angiotensinogen by the action of reninfrom angiotensin I by Angiotensin Converting Enzyme (ACE)release triggered by angiotensin II
effectsnonenonevasoconstriction, increased ADH, increased sympathetic activity, retention of Na+ and water and excretion of K+tubular Na+ and water retention, increased excretion of K+
reduced by drugsproduction reduced by aliskiren (renin inhibitor)production reduced by ACE inhibitors, action reduced by angiotensin II receptor blockersaction reduced by spironolactone
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The RAAS is stimulated in response to hypovolaemia and, specifically, a decrease in renal perfusion. It is a cascade of peptide changes that leads to physiological responses to increase blood pressure and retain sodium and water. In disease such as cardiac failure it is also stimulated and causes fluid retention.

The various components of the RAAS are the targets for a number of drugs used in the treatment of heart failure and hypertension.



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