title: Angiotensin receptor blockers: evidence for preserving target organs.
abstract: Hypertension is a major problem throughout the developed world. Although current antihypertensive treatment regimens reduce morbidity and mortality, patients are often noncompliant, and medications may not completely normalize blood pressure. As a result, current therapy frequently does not prevent or reverse the cardiovascular remodeling that often occurs when blood pressure is chronically elevated. Blockade of the renin-angiotensin system (RAS) is effective in controlling hypertension and treating congestive heart failure. Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) inhibit the activity of the RAS, but these two classes of antihypertensive medications have different mechanisms of action and different pharmacologic profiles. Angiotensin-converting enzyme inhibitors block a single pathway in the production of angiotensin II (Ang II). In addition, angiotensin I is 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 cough 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 the RAS to block the Ang II type 1 (AT1) receptor selectively. Thus, ARBs are more specific agents and avoid many side effects. Experimental and clinical trials have documented the efficacy of ARBs in preserving target-organ function and reversing cardiovascular remodeling. In some instances, maximal benefit may be obtained with Ang II blockade using both ARBs and ACE inhibitors. This review describes clinical trials that document the efficacy of ARBs in protecting the myocardium, blood vessels, and renal vasculature.
authors: Department of Cardiology, Veterans Affairs Medical Center, Washington, DC, USA.
authors: P
authors: P
authors: Carson
authors: T
authors: T
authors: Giles
authors: M
authors: M
authors: Higginbotham
authors: N
authors: N
authors: Hollenberg
authors: W
authors: W
authors: Kannel
authors: H M
authors: HM
authors: Siragy
mesh_terms: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D002908:Chronic Disease; D004359:Drug Therapy, Combination; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy / Q000503:physiopathology; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents