Differential effects of ethanol and mannitol on contraction of arterial smooth muscle.
The present work, using isolated rat aortic strips, indicates that ethanol can inhibit development of spontaneous mechanical activity, induce contractions which are not inhibited by specific amine antagonists and potentiate or inhibit contractions induced by epinephrine and vasopressin. In addition, the data indicate that ethanol can attenuate contractions induced by K+ and can inhibit Ca++-induced contractions of K+-depolarized rat aortic strips. Experiments with a nonpenetrating substance, mannitol, suggest that the effects of ethanol are probably not solely a reflection of hyperosmolarity. Overall, the data could be used to suggest that ethanol may induce hyper- or hypoexcitability of aortic smooth muscle by affecting movement and/or translocation of Ca++.
D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects*; D002118:Calcium / Q000494:pharmacology; D002122:Calcium Chloride / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D000431:Ethanol / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D008353:Mannitol / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects*; D009994:Osmolar Concentration; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D014667:Vasopressins / Q000494:pharmacology
D014667:Vasopressins; D000431:Ethanol; D008353:Mannitol; D011189:Potassium Chloride; D002122:Calcium Chloride; D002118:Calcium; D004837:Epinephrine