The impaired water diuresis of adrenal or pituitary insufficiency is completely corrected by the administration of cortisol and other glucocorti- coid analogues (1-5). This correction results not from improved renal hemodynamics, altered tubular reabsorption of solutes, or removal of a nonosmotic (volume) stimulus to continued antidiuretic hormone (ADH) release, but probably from a direct effect of the steroid on the diluting segments of the nephrons (2, 6). This interpretation implies that the formation, release and in- activation of ADH are normal in the adrenal- insufficient subject. Most of the available data in humans would tend to confirm this implication (1, 2, 5-14). Others, however, have suggested that glucocorticoids may be either biological an- tagonists of or may improve the impaired water excretion in adrenal and pituitary insufficiency by correcting a defect in the metab- olism of ADH
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Kleeman et al. (1960) studied this question.
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