Angiotensin II-Receptor Antagonists: An Overview

Raquel Dina and Mahtab Jafari

Disclosures

Am J Health Syst Pharm. 2000;57(13) 

In This Article

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.[4] 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.[2]

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