Open AccessModulating atherosclerosis through inhibition or blockade of angiotensin
Author(s) -
Rosenson Robert S.
Publication year - 2003
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4950260703
Subject(s) - medicine , angiotensin ii , angiotensin ii receptor type 1 , blockade , angiotensin converting enzyme , bradykinin , heart failure , ace inhibitor , endothelial dysfunction , angiotensin receptor , renin–angiotensin system , myocardial infarction , pharmacology , cardiology , endocrinology , receptor , blood pressure
Angiotensin‐converting enzyme (ACE) inhibitors are well recognized for their benefits in treating hypertension and congestive heart failure and preventing postmyocardial infarction heart failure or left ventricular (LV) dysfunction. Recently, blockade of the angiotensin II type 1 (AT 1 ) receptor was shown to reduce cardiovascular events in hypertensive subjects with LV hypertrophy. Several lines of evidence are now converging to show that ACE inhibitors may affect the atherosclerotic process itself. Emerging clinical data indicate that angiotensin‐receptor blockers (ARBs) may possibly modulate atherosclerosis as well. The antiatherogenic properties of ACE inhibitors and ARBs may derive from inhibition or blockade of angiotensin II, now recognized as an agent that increases oxidative stress. Angiotensin‐converting enzyme inhibition and angiotensin‐receptor blockade also increase endothelial nitric oxide formation, which improves endothelial function. In contrast to the effects of ARBs, the vascular effects of ACE inhibitors may, in part, be mediated by an increase in bradykinin. This article reviews some of the biologic mechanisms whereby ACE inhibitors and ARBs may modulate atherosclerosis.