Early Enhancement of Passive Potassium Efflux from Rat Liver by Thyroid Hormone: Relation to Induction of Na,K-ATPase*

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Abstract
The effect of thyroid hormone treatment on the passive efflux of 42K+ from rat liver slices was studied to determine whether an increase in permeability might play a role in the known enhancement of active monovalent cation transport and Na,K-ATPase activity induced by thyroid hormone. Initial studies showed that the s.c. injection of 50 .mu.g T3[triiodothyronine]/100 g body wt on 3 alternate days resulted in an 82% increase in the 42K+ passive efflux rate constant in liver slices and a 23% increase in the NaK-ATPase activity of liver homogenates. Subsequent investigation of the relative time courses of these 2 hormonal effects showed that after a single injection of T3 the rate constant for 42K+ efflux increased within 6 h and reached a plateau between 24 and 48 h. In contrast, Na,K-ATPase activity was not augmented until 24 h and continued to rise between 24 and 48 h. An early increase in cation permeability (with resultant cation leak) may account for the known stimulatory effect of thyroid hormone on active monovalent cation transport in rat liver. The relatively late increase in Na,K-ATPase activity might then be regarded as an adaptive cellular response to increased passive cation fluxes rather than a direct effect of thyroid hormone. The magnitude and early onset of the effect of thyroid hormone treatment on cellular 42K+ efflux raise the possibility that an increase in passive cation permeability may be a proximal event in the mediation of thyroid hormone action.