Abstract

Glucocorticoids exert tonic suppression of ADH secretion. Hypocortisolism in secondary adrenocortical insufficiency can result in a clinical picture similar to the Syndrome of Inappropriate ADH Secretion (SIADH). On the other hand, in vitro and in vivo results provide evidence for ADH suppression in states of hypercortisolism. 25–45% of the patients with Cushings-Syndrome show symptoms of polyuria/polydipsia. Many patients treated with glucocorticoids for immunosuppression after kidney transplantation also transiently develop polyuria. In both conditions, suppression of ADH may be an important pathogenic factor in addition to direct renal effects. To test the hypothesis that ADH suppression is of relevance during glucocorticoid therapy, we investigated the influence of prednisolone on the osmotic stimulation of ADH. Seven healthy men were subjected to water deprivation tests with the measurement of plasma ADH (pADH) and osmolality (pOsm). Before and after glucocorticoid treatment (five days 30mg prednisolone per day) they were water deprived for eight hours. Before glucocorticoid treatment the probands showed a normal test with an adequate increase of pADH (basal <0.4 to 1.9±0.72 pg/ml [mean±SD]) in relation to pOsm (basal 283.3±8.5 to 293,7±6 mosm/kg). After prednisolone intake, pADH was not stimulated (<0.4pg/ml) in spite of an increase of pOsm from 289.6±4.4 to 296,9±4.7 mosm/kg (p=0.001 for pADH after fluid deprivation with vs. without glucocorticoids). However, urine concentrations increased normally in water deprivation after prednisolone. The increase in urinary cAMP excretion during water deprivation was blunted by prednisolone treatment. Thus, the relation of pADH to pOsm after glucocorticoid intake resembles the situation in patients with central diabetes insipidus. However, after prednisolone treatment, urinary concentrating ability was not impaired, although the increase in urinary cAMP excretion was reduced. We speculate that prednisolone directly stimulated the formation or function of aquaporine channels.

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