Bioscientifica Proceedings

Summary. Concentrations of β-endorphin were quantified in peripheral blood plasma of sheep by a radioimmunoassay that cross-reacted with β-lipotrophin. Plasma concentrations of β-endorphin increased abruptly after physical confinement, bacteraemia, and electroacupuncture treatment for induction of analgesia. In these experimental situations in which plasma concentrations of β-endorphin increased, plasma concentrations of LH often decreased. To test the hypothesis that increases in blood-borne β-endorphin actually caused the decrease in LH release, naloxone was administered to antagonize the opioid receptors at which blood-borne β-endorphin might act. In no case did administration of naloxone disrupt the temporal correlation between experimentally induced increases in plasma β-endorphin and decreases in plasma LH. It was concluded that the increases in blood-borne β-endorphin did not cause the decrease in LH release. Other research investigated whether β-endorphin might be delivered via blood from pituitary to hypothalamus in locally enriched concentrations. Even when pituitary release of β-endorphin was acutely stimulated, it was not possible to demonstrate retrograde delivery of β-endorphin to the hypothalamus without dilution in the systemic circulation. In conclusion, it is unlikely that blood-borne β-endorphin inhibits the release of LH, and β-endorphin should not be classified as a hormone until blood concentrations of the peptide can be shown to exert some effect at a location distant from its site of secretion.

© 1987 Journals of Reproduction & Fertility Ltd