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Adrenocorticotropin and β-Endorphin Release from Rat Adenohypophysis in Vitro: Inhibition by Prostaglandin E₂ Formed Locally in Response to Vasopressin and Corticotropin-Releasing Factor^*

MILA VLASKOVSKA, GEORG HERTTING and WILLHART KNEPEL

Department of Pharmacology, University of Freiburg i. Br. D-7800 Freiburg i. Br., Federal Republic of Germany

Address correspondence and requests for reprints to: W. Knepel, Department of Pharmacology, University of Freiburg, Hermann-Herder-Strasse 5, Freiburg i. Br., D-7800, West Germany.

Abstract

The present study examined the involvement of prostaglandins (PGs) in the mechanisms of ACTH and β-endor-phin release from rat anterior pituitary quarters incubated in vitro. Various cyclooxygenase inhibitors (indomethacin, diclo-fenac, flurbiprofen) had no effect on basal release of ACTH-like or β-endorphin-like immunoreactivity (β-EI), but enhanced ACTH-immunoreactivity/β-EI release upon stimulation by ar-gihine-vasopressin (AVP) or synthetic ovine corticotropin-releasing factor [CRF-(1–41)]. The lowest effective concentration of indomethacin was just sufficient to prevent PG synthesis. Indomethacin was similarly active after blockade of the phos-phodiesterase by 3-isobutyl-l-methylxanthine. When added to the incubation media in concentrations up to 1 µM, PGE₂, D₂, F₂, or prostacyclin (PGI₂) did not alter basal β-EI release; however, with stimulation by AVP or CRF-(1–41), PGE2 but not PGD₂, F₂, or I₂ inhibited β-EI release by about 60%. The concentrations of PGE₂ in the incubation media, as measured by RIA, were somewhat higher than those of any other cyclooxy-genase product (PGD₂, F₂, 6-keto-PGF₁, thromboxane B₂). Upon stimulation by AVP or CRF-(1–41), the concentrations of PGE₂ increased, whereas those of PGD₂ or F₂ remained un-changed. The release of β-EI stimulated by high potassium concentration was not enhanced by indomethacin, although this release was sensitive to inhibition by PGE₂. We conclude that PGE₂ is formed locally subsequent to binding of the neurohor-mones and may act as a negative feedback-modulator of vaso-pressin’s and CRF-(1–41)’s activity in the anterior pituitary gland. (Endocrinology 115: 895–903, 1984)

Footnotes

^* This work was supported by the Deutsche Forschungsgemeinschaft (SFB 70 and Grant Kn 220/1-1).

Supported by an Alexander von Humboldt fellowship. Present address: Institute of Pharmacology, Medical Academy, Sofia, Bulgaria.

Received November 22, 1983.

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