Different receptors mediate morphine-induced prolactin and growth hormone release.
Morphine has a variety of actions on the release of pituitary hormones in addition to its analgesic actions. In the rat, morphine releases prolactin and growth hormone at doses comparable to those active in the tailflick analgesic assay. Naloxazone selectively inhibits the high affinity (mu 1) binding site and dramatically decreases morphine's analgesic potency for over 24 hours. In an effort to determine the opiate receptor mechanisms of morphine-induced prolactin and growth hormone release, groups of rats were treated with either naloxone or naloxazone and 24 hours later the prolactin and growth hormone response to morphine sulfate determined. Peak prolactin levels in the group treated the previous day with naloxone were very similar to levels in untreated controls. However, the peak prolactin levels in the group that received naloxazone the day before were depressed 80% (p less than 0.005). By contrast, growth hormone levels in the naloxazone-treated animals were actually higher than in the naloxone-treated group. Thus prolactin release, like analgesia, appears to be mediated through high affinity, or mu 1, sites, while growth hormone release is not.
D000698:Analgesia; D000818:Animals; D013006:Growth Hormone / Q000097:blood / Q000378:metabolism*; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000031:analogs & derivatives* / Q000494:pharmacology*; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000187:drug effects
D011957:Receptors, Opioid; D009270:Naloxone; C024224:naloxazone; D009020:Morphine; D011388:Prolactin; D013006:Growth Hormone