Giguère V, Labrie F
Biochem Biophys Res Commun. 1983 Jan 27;110(2):456-62. doi: 10.1016/0006-291x(83)91171-3.
The ability of epinephrine to potentiate the action of corticotropin-releasing factor (CRF) was studied in rat anterior pituitary cells in primary culture. Increasing concentrations of epinephrine cause a maximal 6.5-fold stimulation of ACTH release while a 10-fold increase is induced by 5 nM CRF. The two substances exert an additive effect on ACTH release. Although epinephrine alone has no effect on cyclic AMP levels, it causes a maximal 4-fold increase in CRF-induced cyclic AMP accumulation. The stimulatory effect of epinephrine on both parameters is inhibited by the highly specific alpha 1-adrenergic antagonist prazosin but not by the beta-adrenergic antagonist (-)propranolol. Dexamethasone causes a 75% inhibition of ACTH release induced by the combined action of CRF and epinephrine. The present data show that the additive effect of epinephrine on CRF-induced ACTH release is achieved through an alpha-adrenergic receptor and is accompanied by a marked stimulation of intracellular cyclic AMP levels.