TRC: RAAS

RAAS

Renin-angiotensin-aldosteron system (RAAS)

Juxtaglomerular cells in the afferent arterioles release renin in the setting of reduced perfusion pressure, sympathetic activation and decreased delivery of NaCl to the macula densa (tubuloglomerular feedback). The circulating protein angiotensinogen is cleaved by renin to yield angiotensin I. This peptide is further cleaved top angiotensin II by a converting enzyme (ACE) found on the surface of endothelial cells. ACE also degrades bradykinin, a potent vasodilator.

Angiotensin II has several important functions:

stimulation of aldosterone secretion by the adrenal cortex
arteriolar vasoconstriction, which increases blood pressure
direct and indirect (by sympathetic activation) enhancement of NaCl resorption, especially in the proximal tubuli
stimulation of ADH secretion and thirst

Both angiotensin II and aldosterone could be produced locally in tissues contributing to inflammation and fibrosis.

RAAS could be inhibited on several levels by ACE inhibitors, AT-II receptor antagonists and spironolactone. Escape phenomena may explain the usefulness to combine these agents in order to reduce blood pressure and proteinuria.

Elevated levels of the hormones ADH and angiotensin II will produce

Extra info: ADH or vasopressin, as the name tells, increases the resistance of the peripheral vessles and thus increases arterial blood pressure. Angiotensin II is a vasoconstrictor.

Option explanation:

increased peripheral vasodilation

increased peripheral vasoconstriction

increased peripheral blood flow

increased venous return

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

Option explanation:

It increases the production of angiotensin II

It increases the release of aldosterone

It decreases the circulatory volume

It decreases the conversion of angiotensinogen into angiotensin I

RAAS

Renin-angiotensin-aldosteron system (RAAS)

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