Norepinephrine and (Na+, K+)-ATPase: evidence for stabilization by lithium or imipramine.
These experiments examined the effects of lithium and imipramine on the regulation by norepinephrine in vivo of (Na+, K+)-ATPase in brain and heart. The binding of ouabain and the activity of K+-phosphatase were used as indices of (Na+, K+)-ATPase. In the cerebral cortex, imipramine prevented, and lithium reduced, the increase in (Na+, K+)-ATPase associated with repeated injections of yohimbine. Imipramine and yohimbine had synergistic effects on the increased release of norepinephrine and on decreased binding to beta-receptors. Effects on the binding of beta-noradrenergic receptors suggested that imipramine partially reduced stimulation of ATPase by reducing the maximum effect of beta-receptors, while the effect of lithium may have involved a reduction in the exposure of receptors to norepinephrine. Imipramine also increased (Na+, K+)-ATPase in the cerebral cortex of reserpine-treated rats. These results suggest that lithium and imipramine, by different mechanisms, can stabilize fluctuations in the physiological consequences of binding to noradrenergic receptors.
Swann
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AC
Department of Psychiatry, University of Texas Medical School, Houston 77225.
D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism; D004789:Enzyme Activation; D007099:Imipramine / Q000494:pharmacology*; D008094:Lithium / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012110:Reserpine / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D015016:Yohimbine / Q000494:pharmacology
D015016:Yohimbine; D012110:Reserpine; D008094:Lithium; D000254:Sodium-Potassium-Exchanging ATPase; D007099:Imipramine; D009638:Norepinephrine