Earlier studies suggest that cortisol and related glucocorticoids correct the impaired water diuresis of primary and secondary adrenal insufficiency by a direct effect upon the diluting segment of the nephron (1-4); however, no one has conclusively demonstrated that a sustained positive water balance in the adrenal-insufficient patient completely inhibits the secretion of antidiuretic hormone (ADH). Although osmotic inhibition of the release of ADH may be normal in adrenal insufficiency, the human or animal in this state may have a distorted volume stimulus that prevents complete inhibition. Recent studies have demonstrated that contraction or redistribution of both vascular and extracellular volumes can cause the continued secretion of ADH in the water-loaded subject (5, 6). Blood loss, quiet standing, venous congestion of the lower extremities, and positive pressure breathing are all events that may produce this contraction or redistribution. Since the adrenal-insufficient patient is hypo
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Cutler et al. (1962) studied this question.
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