Amaranath L, Anton A H
Arch Int Pharmacodyn Ther. 1977 Nov;230(1):19-30.
Ethanol, like other anesthetics, has been reported to interfere with active Na+ transport in living membranes. In an attempt to elucidate the mechanism by which ethanol exerts this action, we tested in the toad bladder membrane: 1) the effect of ethanol on active Na+ transport, 2) the interaction of ethanol with vasopressin on Na+ transport, and 3) the effect of ethanol on passive Na+ flux. We found that, a) 1-500 microgram/ml of ethanol stimulated, and 10,000 microgram/ml depressed active Na+ transport; b) the combined effect of stimulating concentrations of ethanol and vasopressin, although suggestive of a positive interaction, might have arisen by chance (p = 0.08); c) depressant concentrations of ethanol failed to suppress the stimulation by vasopressin; and d) passive Na+ flux in bladders treated with ouabain and ethacrynic acid was not affected by ethanol (1-100 microgram/ml). These results indicate that ethanol in concentrations ranging from 1 to 10,000 microgram/ml does not block ATP/ATPase Na+ pump but apparently exerts a dose-dependent, stimulant-depressant effect on Na+ channels in the membrane.