Cardiovascular disease, resulting from arteriosclerotic remodeling of the vasculature, is the main cause of death in end-stage renal disease (ESRD) patients. Early during the course of arteriosclerosis, endothelial dysfunction can be detected in various vascular beds, including peripheral forearm arteries, as well as the coronary circulation. Furthermore, endothelial dysfunction seems to predict the prognosis of cardiovascular disease. Therefore, the question deserves attention whether endothelial dysfunction is simply a marker of cardiovascular disease, or an active player in the progress of the disease. A possible link between arteriosclerosis, endothelial dysfunction, and cardiovascular disease is increased oxidative stress. Inflammatory processes involved in the pathogenesis of arteriosclerosis enhance vascular O2- formation, leading to endothelial dysfunction. An activated renin angiotensin system, together with oxidized low-density lipoprotein, may play a prominent role for enhanced vascular oxidative stress. In this context, the endothelium is not only a target of oxygen radicals, but may also contribute to O2- formation. It is the aim of this article to highlight the interplay of inflammation, endothelial dysfunction, and oxidative stress.