17β-estradiol exhibits vasculoprotective effects in vivo. This has been supported by earlier and recent epidemiological data demonstrating greater incidence of atherosclerosis, coronary artery diesease, myocardial infarction, hypertension and other major cardiovascular diseases in man and postmenopausal women compared to premenopausal females. The mechanism(s) of vasculoprotection by estrogens is not known. Presence of the estrogen receptor in the vascular wall makes it feasible that estrogen could exert direct vascular effects and could contribute to the regulation of the cardiovascular system. Nitric oxide, synthesized under physiological conditions by the vascular endothelium, participates in a wide variety of vasculoprotective processes. Based on current evidence from the literature the endothelial constitutive nitric oxide synthase could be a potential target of estrogen's vascular action and may contribute to vasculoprotection by the female sexual steroid hormone.