Chronic ethanol consumption enhances phenylephrine-induced contraction in the isolated rat aorta.
Chronic ethanol consumption contributes to cardiovascular dysfunction possibly related to loss of Mg(2+). This study was designed to examine the role of dietary Mg(2+) supplementation on chronic ethanol ingestion-induced vascular alteration. Rats were fed an ethanol liquid diet supplemented with or without Mg(2+) for 12 weeks. The force-generating capacity was examined in thoracic aortic rings. Ethanol-consuming animals exhibited significantly elevated blood pressure. In aorta with intact endothelium, the contractile responses to norepinephrine and KCl were greatly attenuated and potentiated, respectively. Interestingly, the ethanol-induced alterations in blood pressure and vasoconstrictive response were restored by Mg(2+) supplementation. Pretreatment with the beta(1)-adrenoceptor antagonist atenolol in intact aortic rings abolished the difference in response to norepinephrine between the control and ethanol groups, which implies the involvement of a weakened beta(1)-adrenoceptor component in vessels from the ethanol-fed rats. The norepinephrine-induced vasoconstriction in intact aorta rings was completely abolished by the alpha(1)-adrenoceptor antagonist prazosin. In endothelium-denuded aorta, the contractile response to norepinephrine or KCl was not significantly different between the ethanol and Mg(2+) groups. Endothelium-dependent vasorelaxation to carbamylcholine chloride was not altered by either ethanol or Mg(2+) supplementation. Sodium nitroprusside-induced vasorelaxation was depressed by ethanol, and restored by Mg(2+), in aorta with or without endothelium. These data suggest that chronic ethanol consumption contributes to alterations of endothelium-dependent and -independent vascular response. These alterations can be compensated by dietary Mg(2+) supplementation.