Effect of adenohypophysectomy on salt and water metabolism of the toad Bufo marinus with studies on hormonal replacement

Abstract

Adenohypophysectomy caused a progressive, severe hyponatremia (plasma Na + concentration falling to 65% of the initial value after 20 days). There was a parallel decrease in the exchangeable Na + pool without a concomitant change in Na + space. Adenohypophysectomy also resulted in an increased muscle water content and a decrease in muscle Na + per unit dry weight. Muscle K + decreased on a wet-weight basis only. Plasma K + concentration did not change. Whereas injections of corticosterone, cortisol, or toad pituitary extract prevented the hyponatremia, aldosterone, in a dose of 100 μg/day, was totally ineffective. The treatment of adenohypophysectomized toads with corticosterone resulted in a large weight loss (25% in 20 days), hypokalemia and a decrease in muscle K + content. In addition, urinary nitrogen excretion increased almost two-fold above that of controls. It was concluded that adenohypophysectomy of the toad produced a progressive hyponatremia which was not due to aldosterone deficiency and was correctable by “glucocorticoids.” Administration of aldosterone to intact toads kept in both tap water or 100 meq/liter NaCl did not effect plasma Na + concentration, Na + space or total body Na +. An effect of aldosterone on the renal excretion of Na + could not be demonstrated. In contrast, injection of aldosterone into adenohypophysectomized toads frequently caused a gain in weight and the accumulation of massive edema. Total renal Na + and water excretion, and the minimal Na + concentration of bladder urine, was not modified by adenohypophysectomy. The data suggested that cutaneous Na + handling was interfered with.