Evidence for two differentially regulated populations of peripheral beta-endorphin-releasing cells in humans

M. Michele Murburg, Charles W. Wilkinson, Murray A. Raskind, Richard C. Veith, Daniel M. Dorsa

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

In the current study we tested the hypothesis that human plasma β-endorphin (β E) is derived from at least two subpopulations of β E-releasing cells: one sensitive to glucocorticoids as well as to dopamine (DA; regulated analogously to the corticotrophs of the rat pituitary), and one insensitive to glucocorticoids but sensitive to DA (regulated analogously to the melanotrophs of the rat pituitary). To test this hypothesis, human plasma levels of ACTH, cortisol, and β E-like immunoreactivity were measured at baseline and after haloperidol treatment (0.05 mg/kg, i.v.) in two experimental groups, one pretreated with dexamethasone (1.5 mg) and one pretreated with placebo. Plasma PRL levels were also measured in both groups as an indicator of DA receptor blockade. Dexamethasone partially suppressed both baseline and haloperidol-stimulated levels of human plasma β E-like immunoreactivity, whereas it completely suppressed both basal and haloperidol-stimulated levels of ACTH and cortisol and had no statistically significant effect on either basal or haloperidol-stimulated PRL levels. These data support a negative feedback effect of glucocorticoids on one DA-sensitive cell population that releases both ACTH and β E (corticotroph like), but not on a second cell population that releases β E but not ACTH.

Original languageEnglish (US)
Pages (from-to)1033-1040
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume77
Issue number4
DOIs
StatePublished - Oct 1993

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

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