The prolactin secretory response to β-endorphin and the involvement of opiate receptor subtypes in this response was determined in both diestrous and postpartum, lactating female rats. The involvement of the µ-, δ- and/or ĸ-site was determined by administering specific antagonists for each of these sites prior to β-endorphin. β-Funaltrexamine (β-FNA, 1 or 5 µg) was administered to block µ-sites, ICI 154,129 (5,10 or 25 µg) blocked δ-sites and nor-binaltor-phimine (norBNI, 8 µg) blocked ĸ-sites. The ability of β-FNA and ICI 154, 129 to block prolactin secretion following morphine administration was also determined. A dose response study for β-endorphin indicated that β-endorphin, at doses as low as 25 ng, was a potent stimulus for prolactin release producing an increase in prolactin that mimicked the suckling-induced prolactin increase. In addition, all three antagonists were capable of antagonizing the stimulatory effect of β-endorphin in both diestrous and postpartum female rats. These results indicate that β-endorphin is a potent stimulus for prolactin secretion and that these three opiate receptor subtypes interact to produce its stimulatory effect on prolactin release.

The growth hormone (GH) secretory response to β-endorphin and the involvement of opiate receptor subtypes in this response were determined in diestrous female rats. The involvement of the mu (µ), delta (δ) and/or kappa (K) site was determined by administering specific antagonists for each of these sites prior to β-endorphin. β-Funaltrexamine (1 or 5 µg) was administered to block µ sites, ICI 154,129 (5 or 25 µg) blocked δ sites and nor-binaltorphimine (8 µg) blocked Ksites. The ability of these antagonists to block GH secretion following intravenous morphine administration was also determined. The opiate antagonists and β-endorphin were administered into the lateral ventricle. A dose-response study for β-endorphin indicated that 0.5 µg β-endorphin was the minimum stimulatory dose for GH release, producing an approximately 4-fold increase in circulating levels of GH; lower doses of β-endorphin did not stimulate secretion. All three antagonists were capable of blocking the stimulatory effects of β-endorphin. These results provide evidence that all three opiate receptor subtypes are involved in the stimulatory effect of β-endorphin on GH release.