Abstract
The exaggerated natriuresis of hypothyroid rats receiving a 5% saline infusion was studied to determine the mechanism and the site within the nephron responsible for this increase in sodium excretion. Sodium clearance (C(Na)) and fractional sodium excretion were both demonstrated to be greater in hypothyroid rats for any amount of sodium infused. The rate of increase in fractional sodium excretion in response to saline loading was 3.4 times greater in hypothyroid animals. At the conclusion of the diuresis some of the hypothyroid animals excreted greater than 45% of the filtered sodium load, while no control animal excreted more than 12% of the filtered sodium load. The mean clearance of insulin during the saline diuresis was 36.6% lower (P < 0.001) in the hypothyroid rats. D-Aldosterone given to hypothyroid animals 3 hr before the experiment did not alter the magnitude or rate of increase in fractional sodium excretion. Inulin space determinations in nephrectomized rats revealed that extracellular fluid volume was contracted by 17.1% in the hypothyroid rats (P < 0.01). Plasma sodium was not significantly different in hypothyroid and control animals.A limit on solute free water reabsorption (T(e) (H2O)) per osmolar clearance (C(Osm)) was demonstrated in the hypothyroid rats when these animals excreted greater than 12% of the filtered osmotic load. The limit on T(e) (H2O) formation was associated with an acceleration in the rate of sodium excretion and a decline in the rate of potassium excretion. Early in the diuresis when C(Osm), C(Na), and T(e) (H2O) were comparable in hypothyroid and control rats, the filtered sodium load was 31% lower (P < 0.01) in the hypothyroid animals. These findings indicate that diminished thyroid hormone activity decreases renal sodium reabsorptive capacity. Indirect evidence suggests that the distal and possibly the proximal tubules are the sites of this diminished sodium reabsorption in hypothyroid animals.