Renal Response of Propylthiouracil-Treated Rats to Injected Mineralocorticoids1

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Abstract
Chronic administration of the antithyroid drug, propylthiouracil (PTU), not only induces hypothyroidism but also significantly increases rate of excretion of water and sodium during 5 hr after loading rats with either water or isotonic saline (2.5 ml/100 g body wt ip). After saline loading only, significantly greater amounts of potassium are also excreted. Neither deoxycorticosterone acetate (250 μg/100 g body wt) nor dl-aldosterone (5 μg/100 g body wt), administered prior to water loading, is effective in returning renal sodium loss to the sodium level of euthyroid controls. However, after loading with isotonic saline, both steroids are effective; the minimal doses of aldosterone for significant sodium retention are 0.055 μg/100 g body wt for euthyroid controls and 0.50 μg/100 g body wt for PTU-treated rats. Earlier studies suggested that the increased renal sodium loss of PTU-treated rats could result singly or in combination from: a) decreased renal production of renin and, hence, angiotensin; b) decreased secretion of aldosterone by adrenal cortex; and c) impaired renal response to aldosterone. This study, dealing only with the last, shows that kidneys of PTU-treated rats are capable of responding to exogenous aldosterone, but the threshold for response is elevated approximately 9-fold. (Endocrinology75: 33, 1964)

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