Data are reviewed that suggest that the peripheral vasodilation and hypotension that often result from ingestion (or administration) of ethanol may, in large part, be a consequence of its direct actions on vascular smooth muscle cells, at both the macro- and microcirculatory levels. At lest two mechanisms appear to contribute to this vasodilator effect: 1) inhibition of the normal rhythm or vasomotion (spontaneous mechanical activity) of vascular smooth muscle; and 2) depression of the contractile responses to endogenous neurohumoral substances that play a role in maintaining vascular tone and regulation of blood flow. The information acquired so far suggests that these dilator actions are related causally to interference with movement and/or translocation of Ca2+ across the vascular membranes. Although acetaldehyde and acetate can evoke some actions on isolated blood vessels that somewhat resemble the actions of ethanol, in situ studies on the splanchnic microcirculation reveal that neither acetaldehyde nor acetate can mimic the dilator actions of ethanol on the microvessels. Evidence is also reviewed that indicates that certain concentrations of ethanol, acting on certain peripheral blood vessels (e.g., cerebral and coronary arteries), can induce direct contractile responses (dose-dependent) and potentiate certain hormones, the effects of which are dependent on free, ionized Ca2+ ions. Lastly, data are reviewed in experimental animals, maintained on liquid diets of ethanol, which may provide insights into why a high incidence of hypertensive vascular disease has been noted in alcoholics.