ici-154129 and norbinaltorphimine

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

Topics: Animals; beta-Endorphin; Diestrus; Enkephalin, Leucine; Female; Growth Hormone; Kinetics; Naltrexone; Rats; Rats, Sprague-Dawley; Receptors, Opioid; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu

The prolactin secretory response to beta-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 mu-, delta- and/or kappa-site was determined by administering specific antagonists for each of these sites prior to beta-endorphin. beta-Funaltrexamine (beta-FNA, 1 or 5 micrograms) was administered to block mu-sites, ICI 154,129 (5, 10 or 25 micrograms) blocked delta-sites and nor-binaltorphimine (norBNI, 8 micrograms) blocked kappa-sites. The ability of beta-FNA and ICI 154,129 to block prolactin secretion following morphine administration was also determined. A dose response study for beta-endorphin indicated that beta-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 beta-endorphin in both diestrous and postpartum female rats. These results indicate that beta-endorphin is a potent stimulus for prolactin secretion and that these three opiate receptor subtypes interact to produce its stimulatory effect on prolactin release.

Topics: Animals; beta-Endorphin; Diestrus; Dose-Response Relationship, Drug; Enkephalin, Leucine; Female; Lactation; Male; Naltrexone; Narcotic Antagonists; Prolactin; Rats; Rats, Sprague-Dawley; Receptors, Opioid