Potentiation by steroids of the beta-adrenergic agent-induced stimulation of cyclic AMP in isolated mouse thymocytes.

There is an increasing amount of evidence suggesting that glucocorticoids may modulate the responsiveness of various cell types to beta-adrenergic agents. In some systems, it has been shown, in addition, that steroids potentiate the elevation of cAMP induced by catecholamines. Little is known however of the mechanism underlying steroid action. We have studied this 'permissive action' in isolated thymocytes which have specific receptor sites for both glucocorticoids and beta-adrenergic agents. The glucocorticoid compound dexamethasone did not alter intracellular cAMP level but markedly enhanced the stimulation produced by isoproterenol. This effect was instantaneous and was still measurable at 10(-7) M dexamethasone. A similar potentiating action was observed in the presence of corticosterone but also in the presence of sex steroids. Determination of beta-receptors after cell preincubation in the presence of dexamethasone showed that rapid alterations in beta-receptors are not involved in this permissive action. Experiments done in the presence of the calcium chelator, ethyleneglycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid, suggest that dexamethasone action could be related to a modification of calcium mobilization.