Morphine or capsaicin administration alters the secretion of beta-endorphin into the hypophysial portal vasculature of the rat.

Immunoreactive beta-endorphin (ir-beta-END) concentrations were measured in the hypophysial portal plasma of the male rat under urethane anesthesia. On the basis of immunochemical studies and gel filtration chromatography it appears that ir-beta-END in rat hypophysial portal plasma is primarily beta-endorphin (beta-END) and not beta-lipotropin (beta-LPH). In addition, much of the ir-beta-END in portal plasma may be of pituitary origin since acute hypophysectomy resulted in approximately an 80% decrease in the portal plasma concentration of ir-beta-END. Nevertheless, in anesthetized animals that had been hypophysectomized acutely, portal plasma concentrations of ir-beta-END were still 5 times those in systemic plasma, indicative of hypothalamic secretion of the peptide. The administration of morphine sulfate (3 mg/kg, i.v.) resulted in a decrease of ir-beta-END concentrations from 3,157 +/- 547 pg/ml to 1,044 +/- 250 pg/ml. This effect was blocked by naltrexone (1 mg/kg, s.c.) pretreatment. Capsaicin (10 micrograms), which, when infused into the lateral cerebral ventricle of the rat, has been shown to decrease the amount of beta-END in the hypothalamus, but not elsewhere in the central nervous system, selectively decreased the concentration of ir-beta-END in portal plasma without changing systemic ir-beta-END concentrations. These studies indicate that ir-beta-END in portal plasma is probably beta-END which is derived from neurons in the hypothalamus. Moreover, it is concluded that the regulation of the release of ir-beta-END from these neurons involves opiate receptor mechanisms. The inhibitory influence of opiates on ir-beta-END secretion may be indicative of a classical feedback regulation of ir-beta-END-containing neurons.