Impairment of opioid control of luteinizing hormone secretion in menstrual disorders.
With the aim of examining central opioid influences on the control of luteinizing hormone (LH) secretion, we evaluated the LH response to naloxone, an opioid receptor antagonist, in patients affected by normo-, hyper-, and hypogonadotropic amenorrhea, polycystic ovarian disease and hyperprolactinemia. The results indicate that opioid influences are altered in well-defined pathologic conditions (hyperprolactinemia, obesity), in addition to being modified by gonadal steroids.
D000236:Adenoma / Q000378:metabolism; D000293:Adolescent; D000328:Adult; D000568:Amenorrhea / Q000378:metabolism; D001835:Body Weight; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology / Q000502:physiology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D008599:Menstruation Disturbances / Q000378:metabolism*; D009270:Naloxone / Q000494:pharmacology / Q000502:physiology*; D009839:Oligomenorrhea / Q000378:metabolism; D010053:Ovary / Q000503:physiopathology; D010911:Pituitary Neoplasms / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism
D007987:Gonadotropin-Releasing Hormone; D009270:Naloxone; D011388:Prolactin; D007986:Luteinizing Hormone