Renal tubular sodium reabsorption and oxygen consumption in the hypothyroid dog

The degree to which an insufficiency of thyroid hormone (TH) affects renal tubular sodium reabsorption (RNa) and oxygen consumption (QO2) in vivo, was investigated in a mature mammalian kidney. The results suggest that TH influences renal QO2 as a result of alterations in renal hemodynamics and the renal tubular handling of sodium. Changes in GFR played a major role in the regulation of RNa and QO2. This is suggested by the comparison of hypothyroid animals with and without renal compensatory hypertrophy. In the latter group a twofold lower GFR was associated with parallel changes in RNa and QO2. However, in going from euthyroid (E) to hypothyroid (H) conditions, the decrease in RNa of 31 +/- 4% was greater than the reduction in GFR of 25 +/- 3% (p less than .05). Thus, a decrease in RNa of 6 +- 2% under hypothyroid conditions could not be attributed to the changes in GFR. The normal renal stoichiometry between RNa and QO2 in hypothyroid animals indicates that the above changes in RNa were accompanied by comparable changes in QO2. The decrease in RNa in hypothyroid animals was not associated with a significant change in kidney weight (E:48.2 +/- 4.0gm., n = 5 and H:45.4 +/- 1.4gm, n = 5; pN.S.) The results suggest that an adaptive response to changes in GFR is the predominant cause of the decrease in RNa and renal QO2 under hypothyroid conditions. A modest reduction in renal tubular sodium reabsorptive capacity in hypothyroid animals is probably secondary to a direct effect of TH on active sodium transport.