Different Opioid Mechanisms Are Involved in the Modulation of ACTH and Gonadotrophin Release in Man
作者:
Ashley Grossman,
Peter J.A. Moult,
David Cunnah,
Michael Besser,
期刊:
Neuroendocrinology
(Karger Available online 1986)
卷期:
Volume 42,
issue 4
页码: 357-360
ISSN:0028-3835
年代: 1986
DOI:10.1159/000124463
出版商: S. Karger AG
关键词: Opioids;Cortisol;Adenocorticotropic hormone;Luteinising hormone;Follicle-stimulating hormone;Opioid receptors
数据来源: Karger
摘要:
Both the pituitary-adrenal axis and the pituitary-gonadal axis are under the tonic inhibitory control of endogenous opioid peptides in man. However, the precise opioid receptor involved in the modulation of these hormones remains unknown. The effect of a dose of intravenous naloxone on serum levels of luteinising hormone (LH), follicle-stimulating hormone (FSH) and plasma cortisol was therefore investigated in ten normal subjects. In the male subjects, naloxone at a dose of 25 µg/kg caused a significant increase in serum LH and FSH; no increase in response was seen at the two higher doses (100 µg/kg and 250 µg/kg). The lowest dose (6 µg/kg) caused no change in serum LH and FSH. In the female subjects, tested in the early follicular phase of their cycles, no dose of naloxone significantly increased circulating gonadotrophins. In both male and female subjects, naloxone only stimulated a rise in serum cortisol at the highest dose (250 µg/kg). A second study in six normal subjects demonstrated that the rise in cortisol with the highest dose of naloxone was secondary to a rise in plasma ACTH. It is concluded that the opioid receptor(s) controlling gonadotrophin release in man are naloxone-sensitive, and are probably epsilon-receptors; the naloxone insensitivity of the pituitary-adrenal axis suggests that these responses are modulated by kappa- or delta-recep
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