The renin-angiotensin-aldosterone system (RAAS)

Blood pressure, balance of electrolytes, and circulatory volume are regulated by the renin-angiotensin-aldosterone system. Angiotensin II, aldosterone, and bradykinin are the main actors in this control system. Upon signals of decreasing plasma sodium levels, decreasing circulatory volume, decreasing renal perfusion, decreasing glomerular filtration, or decreasing blood pressure, the kidney releases renin. In the bloodstream, renin converts angiotensinogen from the liver to angiotensin I. Angiotensin-converting enzyme (ACE) from the lungs converts angiotensin I into biologically active angiotensin II. Angiotensin II induces vasoconstriction, stimulates the cells in the zona glomerulosa of the adrenal gland to synthesize and secrete aldosterone, and triggers the kidneys to retain sodium.


Aldosterone indirectly forces the tubular cells in the kidney to reabsorb sodium ions, and as a result, water. All these actions results in increased blood pressure, sodium and water retention, and potassium loss. Angiotensin is also responsible for increasing sympathetic tone and secretion of catecholamines (epinephrine), which also results in vasoconstriction.

The system is regulated a negative feedback mechanism. Besides the conversion of angiotensin I, ACE also inactivates bradykinin, which stimulates the production of vasodilating factors. Hence, vasodilating effects are diminished.


Elevated levels of the hormones ADH and angiotensin II will produce


What is the effect of a high-salt diet on the renin-angiotensin system?


Actions of angiotensin II include: