Acetaldehyde on vascular smooth muscle: possible role in vasodilator action of ethanol

Abstract

Previous studies on intact and isolated blood vessels indicate that ethanol can exert depressant actions on vascular smooth muscle. This study, using isolated rat aortic strips and portal veins, was designed to ascertain whether acetaldehyde (ACT), a major metabolite of ethanol, could exert similar effects. The results indicate that ACT can: (a) inhibit spontaneous mechanical activity and lower baseline tension in aortic strips; (b) depending upon concentration, enhance (abolished by phentolamine) or inhibit such spontaneous contractions in portal veins; (c) dose-dependently attenuate contractions induced by epinephrine, vasopressin, serotonin and KCl; (d) cause non-competitive displacement of the contraction--effect curves of these vasoactive compounds; (e) relax drug-induced contractions of aortic and venous smooth muscle, (f) attenuate Ca2+-induced contractions of K+-depolarized aortas and portal veins. These profound depressant actions of ACT are not attenuated, prevented or mimicked by alpha-adrenergic histaminergic, cholinergic, or serotonergic blocking drugs, nor are they attributable to actions on beta-adrenoreceptors, or release of prostaglandin-like substance. The direct vasodepressant actions of ACT on vascular smooth muscles may play significant roles in alcohol-induced peripheral vasodilatation and hypotension, and cardiovascular collapse noted in the alcohol-Antabuse reaction.