Short term effect of low doses of tri-iodothyronine on proximal tubular membrane Na−K-ATPase and potassium permeability in thyroidectomized rats

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Abstract
Tri-iodothyronine (T3), even when administered for short time and at low doses, induces a large increase in the isotonic fluid reabsorption (J v) in proximal tubules of thyroidectomized rats (TX). In order to investigate the role of the Na−K-ATPase in this process, we measured the Na−K-ATPase activity in early proximal convoluted tubules (S 1) and proximal straight tubules (S 2) microdissected from TX rats and rats treated with low doses of T3 (10 μg/kg body wt), either for 3 days (TX+3T3) or for 7 days (TX+7T3). In both segments no changes in Na−K-ATPase activity were found in TX+3T3 rats versus TX rats, while an increase was registered in TX+7T3 rats. Using micropuncture techniques,J v measured on the same tubular segments increased by 68% in TX+3T3 rats versus TX. Thus, no correlation betweenJ v and Na−K-ATPase activity measured in vitro could be detected after short term treatment of TX rats with T3. Na−K-ATPase activity in vivo is also regulated by the potassium permeability of the membrane, which might be altered by tri-iodothyronine. This hypothesis was tested by perfusing intraluminally and peritubularly proximal tubules of TX rats with the K ionophore, valinomycin (1 μg/ml). In the dual perfusion experiments valinomycin elicited 40% of the action induced onJ v by 3 days treatment with T3. On the other hand, no further increase inJ v was recorded when valinomycin was applied in TX rats pretreated with T3. Taken together, the in vivo and in vitro experiments suggest that low doses of T3 administered for short time to TX rats do not affect Na−K-ATPase activity directly, but stimulate the in vivo activity indirectly by an increase in thek permeability of proximal tubular cell membranes. This latter effect would explain the increase inJ v through an increase in the driving force for sodium entry into the cell.