Glucocorticoid Inhibition of Immunoreactive -Endorphin Release from the Anterior Lobe of the Rat Pituitary: In Vitro and in Vivo Studies

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Abstract
Glucocorticoid control of pituitary .beta.-endorphin (.beta.-END) release was investigated in vitro and in vivo. Cultured cells of rat anterior (AL) and neurointermediate (NIL) lobe released .beta.-END-like immunoreactivity (.beta.-END-LI) in response to epinephrine (10-7 M). However, only the response of AL cells was prevented by corticosterone (10-8-10-6 M) or dexamethasone (10-9-10-7 M). Gel chromatographic analysis (Sephadex G-50) revealed that the major forms of .beta.-END-LI released by AL cells corresponded to .beta.-END and .beta.-lipotropin (.beta.-LPH) in molecular size, whereas virtually all of the immunoreactivity released by NIL cells resembled .beta.-END. In vivo administration of dexamethasone attenuated the stress-induced release of .beta.-END-LI in a dose- and time-related fashion, having a more pronounced effect on plasma levels of .beta.-END-LI corresponding to .beta.-LPH in molecular size. Metyrapone (100 mg/kg), an inhibitor of glucocorticoid synthesis, evoked a rapid (20-40 min) 4- to 6-fold increase in total plasma .beta.-END-LI and 75% of this rise was due to immunoreactivity resembling .beta.-LPH in size. This response was diminished by coadministration of either dexamethasone (0.05-1.25 mg/kg) or corticosterone (0.05-1.25 mg/kg) and completely prevented by 4-h pretreatment with dexamethasone (50 .mu.g/kg). The briskness of the plasma .beta.-END-LI response to acute changes in glucocorticoid status suggested that a rapid feedback mechanism operated in the physiologic control of pituitary .beta.-END-LI secretion. The ability of glucocorticoids to selectively inhibit AL release of .beta.-END-LI in vitro and their pronounced effect on plasma levels of .beta.-END-LI resembling .beta.-LPH, a marker of AL secretion, together indicated that glucocorticoids exerted a selective influence over the secretion of AL corticotrophs in vivo. This demonstration of differential regulation of the AL vs. IL secretion of .beta.-END-LI in vivo most likely reflects a phenomena having biologic importance related to the different physiologic actions of the several molecular forms of .beta.-END-LI secreted by the 2 tissues.

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