Endocrine actions of opioids.
The widespread occurrence of opioid peptides and their receptors in brain and periphery correlates with a variety of actions elicited by opioid agonists and antagonists on hormone secretion. Opioid actions on pituitary and pancreatic peptides are summarized in Table 1. In rats opioids stimulate ACTH and corticosterone secretion while an inhibition of ACTH and cortisol levels was observed in man. In both species, naloxone, an opiate antagonist, stimulates the release of ACTH suggesting a tonic suppression by endogenous opioids. In rats, a different stimulatory pathway must be assumed through which opiates can stimulate secretion of ACTH. Both types of action are probably mediated within the hypothalamus. LH is decreased by opioid agonists in many adult species while opiate antagonists elicit stimulatory effects, both apparently by modulating LHRH release. A tonic, and in females, a cyclic opioid control appears to participate in the regulation of gonadotropin secretion. Exogenous opiates potently stimulate PRL and GH secretion in many species. Opiate antagonists did not affect PRL or GH levels indicating absence of opioid control under basal conditions, while a decrease of both hormones by antagonists was seen after stimulation in particular situations. In rats, opiate antagonists decreased basal and stress-induced secretion of PRL. Data regarding TSH are quite contradictory. Both inhibitory and stimulatory effects have been described. Oxytocin and vasopressin release were inhibited by opioids at the posterior pituitary level. There is good evidence for an opioid inhibition of suckling-induced oxytocin release. Opioids also seem to play a role in the regulation of vasopressin under some conditions of water balance. The pancreatic hormones insulin and glucagon are elevated by opioids apparently by an action at the islet cells. Somatostatin, on the contrary, was inhibited. An effect of naloxone on pancreatic hormone release was observed after meals which contain opiate active substance. Whether opioids play a physiologic role in glucose homeostasis remains to be elucidated.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects; D004723:Endorphins / Q000502:physiology*; D005947:Glucose / Q000378:metabolism; D013006:Growth Hormone / Q000097:blood; D006728:Hormones / Q000378:metabolism*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology; D007986:Luteinizing Hormone / Q000097:blood; D009292:Narcotic Antagonists / Q000627:therapeutic use; D009294:Narcotics / Q000494:pharmacology*; D010187:Pancreatic Hormones / Q000097:blood; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology; D011388:Prolactin / Q000097:blood; D011957:Receptors, Opioid / Q000502:physiology; D013972:Thyrotropin / Q000097:blood; D014667:Vasopressins / Q000097:blood
D004723:Endorphins; D006728:Hormones; D009292:Narcotic Antagonists; D009294:Narcotics; D010187:Pancreatic Hormones; D011957:Receptors, Opioid; D014667:Vasopressins; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D013972:Thyrotropin; D013006:Growth Hormone; D005947:Glucose