Administration of apomorphine (0.3–3.0 mg/kg s.c.) evoked a rapid increase (10 min) in circulating levels of immunoreactive β-endorphin (iβ-END) in rats. As judged by gel filtration chromatography, virtually all of the increase corresponded to iβ-END resembling β-lipotropin (β-LPH) in molecular size. The apomorphine response was inhibited by pretreatment with either the dopamine antagonist, haloperidol (0.1 mg/kg i.p., 2 h) or the glucocorticoid, dexamethasone (50 μg/kg i.p., 4 h). Together, these results indicate that dopamine-receptor activation stimulates the release of opiocortin hormones from corticotrophs of the pars distalis.

Using gel filtration chromatography (Sephadex G-50) and radioimmunoassay for β-endorphin (β-END) and β-lipotropin (β-LPH) we investigated the site [anterior lobe (AL) vs. intermediate lobe (IL)] for serotonergic control of pituitary β-END-like immunoreactivity (β-END-LI) in the rat. Since the secretion of β-LPH in vitro clearly distinguishes β-END-LI release by the AL as compared to the IL, we interpreted changes in plasma levels of immunoreactivity resembling β-LPH to reflect β-END-LI release from the AL. Following the administration of L-tryptophan (200 mg/kg, 30 min, ip), a serotonin precursor, nearly all of the rise in total plasma β-END-LI was due to the form of immunoreactivity resembling β-LPH in molecular size. Similarly, 5-hydroxytryptophan (30 mg/kg, 30 min, ip), a serotonin precursor, and fluoxetine (10 mg/kg, 15 min, ip), a serotonin reuptake blocker, predominantly increased circulating levels of β-LPH-sized immunoreactivity with little effect on β-END-sized immunoreactivity. Quipazine (2.5 and 5.0 mg/kg, 30 min, ip), a serotonin receptor agonist, elevated plasma levels of both forms of β-END-LI; however, the immunoreactive peak coeluting with β-LPH was primarily affected, being increased 9.5-fold while that resembling β-END was increased less than 1-fold.