The angiotensin-converting enzyme (ACE) is a largely tissue-based zinc metalloprotease that regulates the balance between the vasoconstriction and salt retention induced by angiotensin II, via the angiotensin II type 1 (AT1) receptor, and the vasodilator and natriuretic properties of bradykinin. ACE inhibition decreases angiotensin II production and increases bradykinin availability. Since increased ACE is induced in virtually every model of cardiac injury— volume overload, atherosclerotic plaque, infarction, postinfarction remodeling, heart failure, and aging— renin-angiotensin system (RAS) blockade has become the universal first-line strategy. ACE inhibitors may be less specific in their blockade of angiotensin II than AT1 receptor blockers, but they confer valuable cardiovascular protection by increasing the availability of bradykinin. If anything, the bradykinin effect compensates for the incomplete blockade of angiotensin II. ACE inhibitors thus remain the gold standard RAS blocker. Not only have their safety and efficacy been extensively documented, but they confer benefits that are at once biological, structural, and neuroendocrine across diseases as clinically diverse as hypertension, congestive heart failure, ischemic heart disease, myocardial infarction, and diabetic or nondiabetic nephropathy...