Abstract
T renin–angiotensin system is integral to the mechanisms that regulate cardiovascular homeostasis. The renin–angiotensin system has an important role in the pathophysiology of hypertension and heart failure via the vasoconstricting effects of angiotensin II, which sustain elevated blood pressure levels in hypertension and increase afterload in chronic heart failure. Angiotensin II also affects the structure and function of the glomerulus, stimulates the release of aldosterone (causing sodium and water retention), has growth-promoting effects in the myocardium and arterial wall, induces left ventricular hypertrophy, and may mediate proliferative and hypertrophic processes involved in atherosclerosis (Table I).1 Blocking the formation or effects of angiotensin II has important clinical implications for treating cardiovascular diseases and slowing the progression of the cardiovascular disease continuum. The first available class of drugs to affect the renin–angiotensin system was the angiotensin-converting enzyme (ACE) inhibitors. Numerous clinical trials and extensive clinical experience with ACE inhibitors have clearly demonstrated the therapeutic benefits of blocking the conversion of angiotensin I to angiotensin II. More recently, angiotensin II-receptor blockers (ARBs) were introduced for the treatment of hypertension and heart failure. This article provides a brief overview of the pharmacology and clinical use of ARBs with some comparisons to ACE inhibitors.
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