Decreased antidiuretic response to beta-hypophamine in hyperthyroidism.

In the course of studies on the water retention induced by the administration of beta-hypophamine,1 it was noted that a hyperthyroid subject failed to respond to 15 units of Pitressin-tannate-in-oil—a dosage much greater than that causing persistent antidiuresis in normal subjects (1, 2) and in cardiac patients (3). Because this observation supported the concept suggested by some investigators (4, 5), but questioned by others (6), that an antagonism exists between the effects of thyroid and posterior-pituitary hormones on water metabolism, the metabolic response to Pitressin was studied in 4 additional hyperthyroid subjects. The experimental findings indicate that hyperthyroid patients exhibit a greater resistance to Pitressin antidiuresis than can be explained on the basis of either increased total solute excretion or altered renal hemodynamics.