Clonidine releases immunoreactive β-endorphin from rat pars distalis

Abstract

Clonidine (10 −6, 10 −7 M) evokes the release of β endorphin-like immunoreactivity (β-END-LI) from cell cultures of anterior (pars distalis) but not neurointermediate (pars nervosa plus pars intermedia) lobe of the rat pituitary. This drug-induced secretion is blocked by α-adrenergic (phenoxybenzamine, yohimbine; 10 −5 M) but not β-adrenergic (propranolol, 10 −5 M) antagonism. Gel filtration (Sephadex G-50) reveals that β-END-LI released from anterior lobe cells consists of 2 major forms of immunoreactivity which coelute with β-lipotropin or β-endorphin standards. Conversely, β-END-LI released spontaneously from neurointermediate lobe cells almost entirely corresponds to β-endorphin. The data show that α-adrenergic stimulation by clonidine releases β-END-LI selectively from cells of anterior but not neurointermediate lobe in vitro and suggests that the clonidine-induced release of pituitary β-END-LI we have observed in vivo occurs in part by direct action on the corticotrophs of the pars distalis.