(Na+,K+)-ATPase and noradrenergic function: effects of chronic ethanol.
The experiments in this paper examined interactions between ethanol and repeated noradrenergic stimulation in vivo on regulation of (Na+,K+)-ATPase. The increase in ouabain binding and K+-phosphatase activity associated with (Na+,K+)-ATPase in rats treated with repeated yohimbine injections was prevented by chronic ethanol. Ethanol did not affect the yohimbine-induced alterations in noradrenergic receptor binding or in content of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol, showing that prevention of noradrenergic stimulation of (Na+,K+)-ATPase was not caused by a decrease in availability of norepinephrine. In addition, norepinephrine depletion with the neurotoxin DSP4 did not prevent the increases in (Na+,K+)-ATPase indices during chronic ethanol treatment, showing that they did not result from increased norepinephrine exposure. These results suggest that chronic ethanol reduces sensitivity of (Na+,K+)-ATPase to norepinephrine in vivo, possibly as a consequence of membrane effects of ethanol tolerance.
D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D003891:Desipramine / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects; D008297:Male; D009498:Neurotoxins / Q000494:pharmacology; D009638:Norepinephrine / Q000502:physiology*; D010042:Ouabain / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
D001596:Benzylamines; D009498:Neurotoxins; D015016:Yohimbine; D000431:Ethanol; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; C012102:DSP 4; D003891:Desipramine; D009638:Norepinephrine