It is increasingly recognized that sex steroids have, among many other effects, the ability to cause vasodilation. The vasodilatory effects of estradiol have been the best documented and described. At low concentrations, estradiol has the ability to improve impaired endothelium dependent (nitric oxide mediated) relaxation in estrogen deficient subjects. At high concentrations, estradiol causes vasodilation principally by endothelium independent mechanisms, in a gender independent fashion, which appear to involve a number of pathways such as ATP-dependent K+ channels. Testosterone also has ability, at higher doses, to cause vasodilation of the coronary circulation, in a gender independent fashion. The mechanisms of sex steroid-induced vasodilation are reviewed in this article.