Ethanol and contraction of venous smooth muscle

Abstract

Low concentrations of ethanol (17 mM) inhibited development of spontaneous mechanical activity (vasomotion) in isolated rat portal veins. Low concentrations of ethanol potentiated, however, contractions induced by epinephrine, but not those induced by angiotensin or potassium. Higher concentrations of ethanol, such as those associated with surgical anesthesia (100 to 170 mM), resulted in almost complete suppression of spontaneous contractile responses. These higher concentrations of ethanol: attenuate contractions induced by epinephrine, angiotensin, and potassium (K); cause noncompetitive displacement of the dose response curves of these vasoactive compounds; attenuate calcium (Ca) induced contractions of K depolarized portal veins; relax drug induced, as well as Ca induced, contractions of portal veins. The profound depressant actions of ethanol are not mimicked by alpha adrenergic, histaminergic, cholinergic, or serotonergic blocking drugs, nor are they attributable to actions on β adrenergic receptors. The direct vasodepressant actions of ethanol on isolated venous smooth muscle may play a significant role in alcohol induced peripheral vasodilatation seen in man and animals.