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As part of the systemic circulating human renin– angiotensin system, angiotensin 1-converting enzyme (ACE) degrades (vasodilator) kinins and generates (vasoconstrictor) angiotensin II. Angiotensin II also drives adrenal aldosterone production, leading to salt and water retention. Pharmacological inhibition of ACE activity has thus found its place in the management of both heart failure and hypertension, with a cumulative worldwide experience of more than 200 million patientyears of treatment. However, the reductions in cardiovascular mortality and morbidity associated with such therapy far exceed those anticipated for a mere vasodilating natriuretic, benefits which have yet to be adequately mechanistically explained. In recent years, however, it has become increasingly clear that local tissue renin–angiotensin systems also exist in diverse tissues, whose influence on tissue physiology and pathophysiology has become the subject of intense research efforts. It is postulated that a reduction in tissue ACE activity, rather than that in the circulation, might underlie the beneficial effects of ACE inhibitor therapy. ACE activity in both circulating (endocrine) and local (autocrine or paracrine) systems is under strong genetic influence. The existence of a single major genetic influence on circulating ACE levels was first suggested by Cambien and colleagues in 1988. Only 2 years later, and this genetic influence was shown to be the ACE gene itself: the absence (deletion, D) rather than the presence (insertion, I) of a 287 base pair marker was associated with significantly higher circulating ACE levels. Not long afterwards, the ACE I/D polymorphism was shown

Is genotype or phenotype the better tool for investigating the role of ACE in human cardiovascular disease?