Abstract
Angiotensin converting enzyme (ACE) inhibitors have proved effective in preventing or ameliorating clinical manifestations of atherosclerosis, such as myocardial infarction (MI) and heart failure. Experimental evidence demonstrates their anti-atherogenic potential; ACE inhibitors do not only suppress the formation of proatherogenic angiotensin II (AII), but also enhance the formation and release of anti-atherogenic nitric oxide (NO) at local tissue sites; both mechanisms are implicated in the suppression of neointima formation in the balloon-injured vessel wall. A similar anti-atherogenic potential is provided by the blockade of the renin-angiotensin system (RAS) at the level of the angiotensin type-1 (AT1) receptor. AT1 receptor antagonists do not only block the proatherogenic actions of AII, but also induce an enhanced formation and release of anti-atherogenic NO at local tissue sites. AT1 receptor antagonists may therefore prove as effective as ACE inhibitors in patients with manifest atherosclerosis.