Ethyl alcohol interferes with excitation-contraction mechanisms of canine antral muscle.
Ethyl alcohol (EtOH) inhibited spontaneous and acetylcholine (ACh)-induced contractions in a dose-dependent manner (0.1-2.5%). These concentrations also reduce the amplitudes of intracellularly recorded slow waves. The effects of EtOH do not appear to be mediated by adrenergic or prostaglandin mechanisms, nor can they be explained on the basis of hyperosmolarity. At higher concentrations (1-10%), EtOH totally abolished phasic contractile activity and caused tonic contraction. ACh was not able to restore normal phasic contractions to muscles treated with EtOH above 2.5% and, in fact, further enhanced the force of the tonic contraction. The membrane potential response to EtOH above 1% was biphasic; the membrane transiently hyperpolarized and then tonically depolarized. It appears that many of the effects of EtOH on gastric emptying might be due to direct interference by EtOH in the membrane events leading to excitation-contraction coupling in gastric smooth muscle.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D008297:Male; D008564:Membrane Potentials; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011706:Pyloric Antrum / Q000502:physiology*
D000431:Ethanol; D011433:Propranolol; D000109:Acetylcholine; D009638:Norepinephrine; D010646:Phentolamine