ACE-Gene Polymorphism and Endothelial Dysfunction in Normal Humans

To the Editor: Recently, Butler et al1 have reported that the DD angiotensin-converting enzyme (ACE) genotype in a young normal population is associated with a blunted vasodilator response both to acetylcholine (ACh) and sodium nitroprusside. These data disagree with findings previously reported by ourselves.2 In fact, in our article, we demonstrated that hypertensive patients with the DD genotype are characterized by significantly less endothelium-dependent vasodilation in comparison with ID and II genotypes, but normal control subjects with a DD genotype had similar endothelium-dependent vascular responses when compared with the non-DD genotypes.Moreover, no significant differences were observed in endothelium-independent vasodilation between normal subjects and hypertensive patients. Similarly, no significant differences were detected when we subdivided the control and hypertensive groups according to ACE-gene genotypes. Methodological differences and population selection criteria may explain the following disparate findings:(1) The authors demonstrated both an impaired endothelium-dependent (ACh) and an endothelium-independent (nitroprusside) vasodilation. These data are in opposition to results reported by many authors who demonstrated, obviously, any difference in endothelium-independent vasodilation between normal controls and patients with endothelial dysfunction due to hypertension, diabetes, aging, …