title: Dietary Mg(2+) supplementation restores impaired vasoactive responses in isolated rat aorta induced by chronic ethanol consumption.
abstract: 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.
authors.affiliation: Department of Biology, Morgan State University, Baltimore, MD 21251, USA.
authors.forename: Ricardo A
authors.initials: RA
authors.lastname: Brown
authors.forename: Karl J
authors.initials: KJ
authors.lastname: Ilg
authors.forename: Alex F
authors.initials: AF
authors.lastname: Chen
authors.forename: Jun
authors.initials: J
authors.lastname: Ren
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000502:physiology; D001262:Atenolol / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000502:physiology; D000431:Ethanol / Q000008:administration & dosage*; D005260:Female; D066298:In Vitro Techniques; D008274:Magnesium / Q000008:administration & dosage*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D000431:Ethanol; D001262:Atenolol; D011189:Potassium Chloride; D008274:Magnesium; D009638:Norepinephrine; D011224:Prazosin