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