Release of dynorphin-like immunoreactivity from rat adenohypophysis in vitro during inhibition of anterior pituitary hormone secretion from individual cell types

M. Schwaninger, W. Knepel*, K. D. Da–Hler, J. Sandow

*Corresponding author for this work
8 Citations (Scopus)

Abstract

LHRH has previously been found to be the only known hypothalamic releasing factor which can specifically stimulate the release of the opioid dynorphin and other proenkephalin B-derived peptides from the rat adenohypophysis in vitro. In the present study the mechanisms that regulate dynorphin release were further characterized. It was examined whether or not dynorphin release from the adenohypophysis in vitro is altered during inhibition of the secretion of various anterior pituitary hormones. Rat anterior pituitary quarters were incubated in vitro and hormone release into the incubation medium was measured by RIAs. Somatostatin, dopamine, T3, dexamethasone, and 5a-dihydrotestosterone were used to inhibit the secretion of GH, PRL, TSH, ACTHβ-endorphin, or LH/FSH, respectively. GH, PRL, or 0-endorphin release was inhibited without affecting the simultaneous release of dynorphin A-(1–3)-like immunoreactivity (Dyn A1–3-IR). Concentrations of T3, somatostatin, or dopamine which were effective in suppressing the evoked and/or basal release of TSH, GH, or PRL, respectively, produced no effect on Dyn A1–3-IR release caused by high potassium concentration (40 mMJ or LHRH (500 pM). The LHRH-induced release of LH and FSH was inhibited by the glucocorticoid dexamethasone or the androgen 5α-dihydrotestosterone. Under these conditions, Dyn A1–3-IR release was also reduced. However, whereas LH release was completely blocked by 5α-dihydrotestosterone, FSH and Dyn A1–3-IR release was reduced only by 50%. The release of FSH and Dyn A1–3R in vitro from anterior pituitary glands taken from rats, castrated 3 weeks before, was enhanced to a similar extent (about 2.5-fold); the simultaneous enhancement of LH release was significantly (P < 0.005) greater (about 5-fold). We conclude that the mechanisms which regulate the release and/or biosynthesis of dynorphin and other proenkephalin B-derived peptides of the adenohypophysis are similar to those of the gonadotropins but different from those of any other anterior pituitary hormone, and may be more closely related with FSH release than LH release. These data support the view that dynorphin of the normal rat adenohypophysis may be localized in at least a subpopulation of gonadotrophs.

Original languageEnglish
JournalEndocrinology
Volume121
Issue number1
Pages (from-to)167-174
Number of pages8
ISSN0013-7227
DOIs
Publication statusPublished - 07.1987

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)

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