Angiotensin receptor blockers: Evidence for preserving target organs

Hypertension is a major problem throughout the developed world. Although cu rrent antihypertensive treatment regimens reduce morbidity and mortality, p atients are often noncompliant, and medications may not completely normaliz e blood pressure. As a result, current therapy frequently does not prevent or reverse the cardiovascular remodeling that often occurs when blood press ure is chronically elevated. Blockade of the renin-angiotensin system (RAS) is effective in controlling hypertension and treating congestive heart fai lure. Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin r eceptor blockers (ARBs) inhibit the activity of the RAS, but these two clas ses of antihypertensive medications have different mechanisms of action and differ ent pharmacologic profiles. Angiotensin-converting enzyme inhibitor s block a single pathway in the production of angiotensin II (Ang TT). In a ddition, angiotensin Iis not the only substrate for ACE. The ACE inhibitors also block the degradation of bradykinin that may have potential benefits in cardiovascular disease. Bradykinin is, however, the presumed cause of co ugh associated with ACE inhibitor therapy. Data from clinical trials on ACE inhibitors serve to support the involvement of the RAS in the development of cardiovascular disease. Angiotensin receptor blockers act distally in th e RAS to block the Ang II type 1 (AT(1)) receptor selectively. Thus, ARBs a re more specific agents and avoid many side effects. Experimental and clini cal trials have documented the efficacy of ARBs in preserving target-organ function and reversing cardiovascular remodeling. In some instances, maxima l benefit may be obtained with Ang LI blockade using both ARBs and ACE inhi bitors. This review describes clinical trials that document the efficacy of ARBs in protecting the myocardium, blood vessels, and renal vasculature.