Concentrations of beta-endorphin were measured in the venous effluent of the hypothalamus (hypophyseal portal blood) at various phases of the menstrual cycle and after ovariectomy in rhesus and pigtailed monkeys. In the rhesus, beta-endorphin concentrations were high during the mid- to late follicular phase [737 +/- 256 pg/ml (mean +/- SE)] and the luteal phase (1675 +/- 1108) of the menstrual cycle, but were undetectable (less than 133) at menstruation. Concentrations were also high in pigtailed monkeys during stages of the menstrual cycle other than at menstruation (4870 +/- 1090 pg/ml), but undetectable (less than 133) 4--12 months after ovariectomy. These results indicate that beta-endorphin concentrations in hypophyseal portal blood are related to menstrual cycle events, probably changes in ovarian steroids; this in turn suggests that beta-endorphin may participate in the ovarian feedback regulation of gonadotropin secretion.
PMID 6286285 6286285 DOI 10.1210/endo-111-3-879 10.1210/endo-111-3-879
Cite this article
Wehrenberg, W. B., Wardlaw, S. L., Frantz, A. G., & Ferin, M. (1982). beta-Endorphin in hypophyseal portal blood: variations throughout the menstrual cycle. Endocrinology, 111(3), 879-881. https://doi.org/10.1210/endo-111-3-879
Wehrenberg WB, Wardlaw SL, Frantz AG, Ferin M. beta-Endorphin in hypophyseal portal blood: variations throughout the menstrual cycle. Endocrinology. 1982;111(3):879-881. doi:10.1210/endo-111-3-879
Wehrenberg, W. B., et al. "beta-Endorphin in hypophyseal portal blood: variations throughout the menstrual cycle." Endocrinology, vol. 111, no. 3, 1982, pp. 879-881.
beta-Endorphin has a role in the regulation of the normal menstrual cycle and possibly in the onset of puberty. We have reviewed the evidence pointing to an alteration in this neuropeptide that may contribute to the pathogenesis of various reproductive dysfunctions. Elevated or high levels of beta-endorphin have been associated with exercise-associated amenorrhea, stress-associated amenorrhea, and polycystic ovarian syndrome. Depressed or low levels of beta-endorphin have been associated with PMS and menopause. Alterations in the levels of beta-endorphin may change the pulsatile release of GnRH via noradrenergic and/or dopaminergic pathways. We have primarily focused on beta-endorphin as representative of the endogenous opioid peptides, but other opioid peptides may also contribute to the pathogenesis of various types of reproductive dysfunction. Perhaps it will become possible to characterize and hone our understanding of the function of beta-endorphin and the other substances composing the endogenous opioid peptides. A better understanding of their role in physiological as well as pathophysiological processes may allow for the development of rational approaches to the treatment of specific disorders pertaining to reproduction. Many questions remain unanswered. what is the precise mechanism of action by which beta-endorphin exerts its influence on pulsatile GnRH release? Is there a functional relationship between CNS and peripheral (serum) levels of beta-endorphin? Are the detected changes in beta-endorphin levels merely associated, or are they a cause of a particular disorder? Since it took almost 40 years between the time prostaglandins were first discovered and eventual realization of their clinical application, it may take some time before the beta-endorphin story is complete.
Journal Article THE NEUROENDOCRINOLOGY OF OPIOID PEPTIDES Get access ASHLEY GROSSMAN, BA BSc MRCP, ASHLEY GROSSMAN, BA BSc MRCP Departments of Endocrinology and Chemical Endocrinology St Bartholomew's Hospital, London Search for Oxford Academic PubMed Google Scholar LESLEY H REES, MD MSc MRCPath FRCP LESLEY H REES, MD MSc MRCPath FRCP Departments of Endocrinology and Chemical Endocrinology St Bartholomew's Hospital, London Search for Oxford Academic PubMed Google Scholar British Medical Bulletin, Volume 39, Issue 1, 1983, Pages 83–88, //doi.org/10.1093/oxfordjournals.bmb.a071796 01 March 1983
The concentration of human beta-endorphin (beta h-EP)) was measured in various hypothalamic nuclei, in extrahypothalamic brain regions and in the anterior and posterior lobes of the pituitary using a specific radioimmunoassay (RIA) The beta h-EP concentrations in the arcuate nucleus (169 +/- 35 pg/100 micrograms protein, n = 7) and median eminence (163 +/- 32 pg/100 micrograms protein, n = 6) were among the highest in the 17 brain areas examined. The immunoreactive beta h-EP in the hypothalamus corresponded to authentic beta h-EP, as determined by gel exclusion chromatography. By chromatography and RIA the beta h-EP concentrations in anterior (1.53 X 10(5) +/- 0.51 X 10(5) pg/100 micrograms protein, n = 3) and posterior (1.41 X 10(5) +/- 0.38 X 10(5) g/100 micrograms protein, n - 5) pituitary were found to be approximately 1,000-fold higher than in hypothalamus. Within the pituitary beta h-EP was localized throughout the anterior lobe, in the pars intermedia and in that part of the posterior lobe nearest the pars intermedia, as judged by immunocytochemistry. Dense immunocytochemical staining was found along the perimeter of many blood vessels. Beta h-EP and adrenocorticotropin (ACTH) were co-localized in the same pituitary cells. The present data represent the first unequivocal localization and quantitation of beta h-EP in human brain and in the separate lobes of the human pituitary.