Abstract-Black Africans have a higher incidence of cardiovascular disease than white Europeans. We explored potential mechanisms of this excess risk by assessing endothelium function, inflammatory status (C-reactive protein), oxidative stress (isoprostane-F2␣), and plasma asymmetrical dimethyl arginine (ADMA; an endogenous competitive inhibitor of NO synthase) in each ethnic group. 1 This in part may be explained by an increased prevalence and severity in blacks of some risk factors for atherosclerosis. In particular, in black subjects, essential hypertension has a higher prevalence, earlier onset, and is associated with more severe end-organ damage, including left ventricular hypertrophy, renal failure, and stroke. 1 However, conventional risk factors for cardiovascular disease do not account for all of this increased risk. A recent study demonstrated that black ethnicity is a strong and independent risk factor for the development of peripheral arterial disease, which was not explained by higher levels of diabetes, hypertension, or body mass index. 2 The mechanisms underlying this ethnic predisposition to cardiovascular dysregulation remain unresolved.A number of studies have demonstrated that black subjects have endothelial dysfunction, 3-5 a key step in the initiation/ progression of atherosclerotic vascular disease. A hallmark of endothelial cell dysfunction is a reduction in the bioavailability of the antiatherosclerotic signaling molecule NO. 6 Longitudinal studies have demonstrated that a reduction in NO bioavailability is a predictor of accelerated atherosclerosis. 7,8 NO is generated by a family of NO synthases from L-arginine in a reaction that requires oxygen, reduced nicotinamideadenine dinucleotide phosphate, and essential cofactors, including tetrahydrobiopterin. NO bioavailability is principally determined by a reduction in its biosynthesis and/or inactivation by reactive oxygen species. Asymmetric dimethylargi-