Netchitailo P, Lihrmann I, Vaudry H
J Steroid Biochem. 1984 Dec;21(6):727-31. doi: 10.1016/0022-4731(84)90037-2.
Previous studies have demonstrated the presence of glucocorticoid receptors in the adrenal gland and suggested a direct inhibitory effect of glucocorticoids on the adrenal cortex. The present study was designed to investigate the possibility that dexamethasone could inhibit adrenal steroidogenesis in amphibia. For this study, we have applied a well-defined perifusion model, using interrenal fragments from frogs (Rana ridibunda). The amounts of corticosterone and aldosterone released in the effluent perifusate were radioimmunoassayed by means of specific antisera which did not cross-react with dexamethasone. Administration of dexamethasone (10(-6) and 10(-5M) did not significantly alter the basal secretion of corticosterone and aldosterone. In addition, dexamethasone (10(-5)M) did not modify the response of the interrenal gland to graded doses of ACTH. Finally dexamethasone did not inhibit the stimulation of corticosterone and aldosterone production induced by a single infusion of the angiotensin II analogue [Sar1-Val5] AII. From these results, it is concluded that in amphibia, chronic dexamethasone administration does not exert a direct suppressive effect on adrenal secretion.