Evidence for Independent Secretion of β-Endorphin Immunoreactivity from Rat Pars Distalis in Vivo

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Abstract
The distinctive chromatographic patterns of β-endorphin-like immunoreactivity (βEND-LI) released from rat pars distalis (PD) or pars intermedia in vitro as well as the selective inhibitory effects of dexamethasone on PD were used to determine which lobe secretes (βEND-LI into plasma after clonidine administration in vivo. Gel chromatography (Sephadex G-50) indicates that cultured PD cells released two major immunoreactive species which coelute with β-ipotropin (βLPH) or βEND standards. Conversely, virtually all of the βEND-LI secreted by neurointermediate lobe [pars intermedia plus pars nervosa (NIL)] cells in vitro resembled βEND in size, while none was detected which cochromatographed with βLPH. Incubation of PD cells with clonidine (10-6 M) evoked a 2-fold increase in βEND-LI release, while the drug had no effect on βEND-LI released from cultured NIL cells. Dexamethasone (10-7 M) inhibited the clonidine-induced release of βEND-LI from PD cells, whereas it did not influence the stimulated release of βEND-LI from NIL by isoproterenol (10-6 M). In vivo administration of clonidine (0.5 mg/kg, ip, for 15 min) increased total plasma βEND-LI from 0.75 plusmn; 0.16 to 1.35 ± 0.18 ng/ml; 85% of this rise corresponded to βLPH as determined by gel chromatography. Prior administration of dexamethasone (60 μg/kg, ip, for 4 h) completely prevented the clonidine-induced release of βEND-LI in vivo. These results demonstrate that clonidine probably acts selectively on the PD in vivo to release pituitary βEND-LI, and further, that PD can release βEND-LI independently of the pars intermedia.