The Renin-Angiotensin Receptor System
The renin-angiotensin-aldosterone cascade is activated when renin, secreted by the juxtaglomerular cells of the kidneys, catalyzes the conversion of angiotensinogen to angiotensin I (AT-I) in the liver. AT-I is locally transformed into active AT-II via ACE. AT-II, a peptide hormone, is responsible for numerous effects: aldosterone production and release, afferent and efferent vasoconstriction, proximal tubular reabsorption of sodium, increased inotropism and chronotropism, stimulation of drinking behavior and sodium appetite, vagus suppression, and b-adrenergic-receptor stimulation. Two subtypes of AT-II receptors have been identified. Type 1 receptors are predominantly found on vascular endothelium and are linked to all the known physiological and pharmacologic actions of AT-II. Stimulation of type 1 receptors by AT-II induces vasoconstriction, renal tubular sodium reabsorption, aldosterone release, vascular smooth muscle remodeling, and stimulation of central and peripheral sympathetic activity, thus leading to increases in blood volume and blood pressure. Antagonism of type 1 receptors lowers blood pressure by inhibiting these actions. Type 2 receptors are predominantly found in the adrenal medulla, uterus, and fetal tissue and may play a role in fetal growth and differentiation, although the exact function of these receptors has not been identified.
Am J Health Syst Pharm. 2000;57(13) © 2000 American Society of Health-System Pharmacists
Cite this: Angiotensin II-Receptor Antagonists: An Overview - Medscape - Jul 01, 2000.