This chapter discusses the mechanism of action of angiotensin II (AII). The octapeptide AII is the primary effector hormone of the rennin-angiotensin-aldosterone system, regulating not only the release of aldosterone from the adrenal but also that of renin from the kidney. By inhibiting the secretion of renin—the enzyme which catalyses the proteolysis of angiotensinogen to the AII-precursor angiotensin I (AI)—AII effectively regulates its own formation as well via a negative feedback loop. AII receptors have also been identified in the kidney, brain, uterus, placenta, pituitary, and reticuloendothelium. Saturable binding of radiolabeled AII is demonstrable in adrenal glomerulosa, vascular smooth muscle, and hepatic plasma membranes. In some smooth-muscle cell types, AII alters the activity of both phospholipase C and adenylate cyclase, presumably via a single-receptor type. The biological effect of AII on its target tissues can be altered by changing either receptor affinity or receptor number. In the adrenal, liver, and vasculature the affinity of the receptor for AII is modulated by cations, such as sodium, calcium or magnesium, and by reducing agents.
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