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.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D001667:Binding, Competitive; D000242:Cyclic AMP / Q000096:biosynthesis; D004082:Dihydroalprenolol / Q000378:metabolism / Q000494:pharmacology; D004357:Drug Synergism; D004837:Epinephrine / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology*; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000378:metabolism
D000318:Adrenergic beta-Agonists; D011943:Receptors, Adrenergic, beta; D004082:Dihydroalprenolol; D000242:Cyclic AMP; D006854:Hydrocortisone; D004837:Epinephrine