DECREASED ANTIDIURETIC RESPONSE TO BETA-HYPOPHAMINE IN HYPERTHYROIDISM*

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Abstract
In contrast to normal subjects and cardiac patients, 3 severely hyperthyroid patients on regular Na intakes failed to achieve the anticipated anti-diuresis and increase in urinary total solute concentration, when given 2-15 units of beta-hypophamine in the form of Pitressin-Tannate-in-Oil (PTO) daily for 6 to 12 days. Two other hyper-thyroid patients on low Na diets also exhibited diminished responsiveness to PTO. Following successful treatment with I131, one patient showed a normal antidiuretic response to PTO. In one of these subjects, intravenous administration of physiologic doses of aqueous Pitressin also failed to induce acute antidiuresis, comparable to that observed subsequently when she was euthyroid following I131 therapy. The observation that a normal response to PTO was obtained in a euthyroid subject whose urinary solute excretion was markedly augmented by increased oral intakes of NaCl and N suggests that increased urinary total solute loads alone cannot explain the apparent resistence of hyperthyroid patients to beta-hypophamine.