Thyroid calorigenesis in isolated, perfused rat liver: minor role of active sodium‐potassium transport.

Abstract

The effects of ouabain of hepatic O2 uptake, cell membrane potential, and Na-K transport were examined at 37.degree. C during nonrecirculating perfusion of isolated livers from fasted normal rats and rats treated with triiodothyronine (T3). The perfusate was Krebs-Ringer bicarbonate buffer containing albumin and bovine erythrocytes. Treatment with T3 increased the rate of hepatic O2 uptake by 30% (i.e. by 0.83 (.mu.mol/min) O2 g liver). After shifting to perfusate containing 2.5 mM ouabain, a 4-5 mV depolarization and maximal rates of net hepatic K release and Na uptake occurred within 2 min in both thyroid states. These changes were not accompanied by any significant change in the rates of hepatic O2 uptake. T3-treatment increased the maximal, post-ouabain net flux of K by 29% (i.e. by 0.52 (.mu.eq/min) per g liver). The T3-induced increase in the net flux of Na (19%) did not achieve statistical significance. In either thyroid state, the observed passive fluxes of Na and K were calculated to be balanced by active fluxes at the expense of 5-6% of the observed rate of hepatic O2 uptake. Hyperthyroidism may enhance the rate of hepatic Na-K transport, but the energy expenditure due to this process appears to be too small to make any important contribution to thyroid calorigenesis in perfused rat liver.