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The exact mechanism (s) responsible for the impaired water diuresis of primary and secondary adrenal cortical insufficiency is still unknown. Previous studies from this (1-3) and other laboratories (4-6) have suggested that this defect is due in part to the loss of a permissive effect of cortisol-like steroids on the diluting segments of the nephron, i.e., a normal amount of glucocorticoid is essential to allow maximal impermeability to water to develop in these segments in the absence of circulating antidiuretic hormone (ADH). This concept implies that the release, metabolism, and action of ADHare normal in the adrenal-insufficient patient (1-3). Others (7-12), however, imply that adrenal glucocorticoids directly affect the release and metabolism of ADH. This implies that the impaired water diuresis of adrenal insufficiency is due to the altered ADHphysiology or its unopposed activity. These conflicting points of view have in general developed from experiments in which the release, metabolism, and action of ADH were studied indirectly rather than by direct measurement of the hormone in biologic

the journal of clinical investigation/the journal of clinical investigation

Mechanisms of Impaired Water Excretion in Adrenal and Pituitary Insufficiency. IV. Antidiuretic Hormone in Primary and Secondary Adrenal Insufficiency *