Lack of stimulation of renal (Na+ +K+)-ATPase by thyroid hormones in the rabbit.

The effect of 1-3,5,3'-triiodothyronine (T3) and thyroxine (T4) on (Na+ +K+)-ATPase activities was examined in rabbit kidneys because in this tissue almost 80% of the metabolism is connected to active sodium transport. T3-receptor concentrations were estimated as 0.62 and 0.80 pmol/mg per DNA in the cortex and outer medulla, respectively. A dose of 0.5 mg T3/kg body weight for 3 days increased basal metabolic rate by almost 60%, and the mitochondrial 1-alpha-glycerophosphate dehydrogenase activity was increased by 50% in both the cortex and medulla. (Na+ +K+)-ATPase activity in the liver was raised by almost 50%. However, no changes in (Na+ +K+)-ATPase activities or binding sites for [3H]ouabain in either the kidney cortex or medulla could be observed. T4 at 16 mg/kg daily for 14 days was also without effect on renal (Na+ +K+)-ATPase activities. Furthermore, the response to T3 was absent at high sodium excretion rates induced by unilateral nephrectomy and extracellular volume expansion. Thus, despite stimulation of basal metabolic rate and renal 1-alpha-glycerophosphate dehydrogenase activity by T3 and T4, the (Na+ +K+)-ATPase activity in the rabbit kidney is identical in euthyroid and hyperthyroid states. However, thyroid hormones prevent the normal natriuretic response to extracellular volume expansion.