Hydrocortisone increases the responsiveness of mast cells to beta-adrenergic agonists by an action distal to the beta-adrenoreceptors.

Hydrocortisone in pharmacologically attainable concentrations potentiates beta-adrenergic-stimulated cyclic AMP accumulation in rat peritoneal mast cells. Direct binding studies using 3H-dihydroalprenolol indicated no significant changes in the number of beta-adrenoreceptors or in the kinetics of the interaction of the radio-ligand with receptors after treatment of mast cells with the corticosteroid. Competition binding studies with epinephrine revealed no hydrocortisone-induced change in Kd values for this agonist. It is concluded that hydrocortisone-induced stimulation of cyclic AMP synthesis results from an effect that occurs beyond the interaction of the beta-adrenergic agonist with its receptor.