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5-Hydroxyeicosatetraenoic Acid Increases Prolactin Release from Rat Anterior Pituitary Cells^*

K. KOIKE, A. M. JUDD and R. M. MACLEOD

Department of Medicine, University of Virginia School of Medicine Charlottesville, Virginia 22908

Abstract

The enzymatic breakdown of phospholipids to form arachidonic acid and its subsequent conversion to metabolites produced via the lipoxygenase pathway in anterior pituitary cells may contribute to the process of PRL release. The incubation of primary cultures of pituitary cells from female rats with the lipoxygenase product 5-hydroxyeicosatetraenoic acid (5-HETE; 5–100 µM) significantly increased PRL release in a concentration-dependent manner. The release of PRL induced by 45 µM 5-HETE was completely blocked by 1 µM dopamine. Penfluridol, an agent that binds to and inactivates several Ca⁺²- binding proteins, including calmodulin, decreased (P < 0.01) basal and 5-HETE-stimulated PRL release. Similarly, 50 µM D-600, a Ca⁺² channel antagonist, significantly (P < 0.01) reduced basal and 5-HETE-induced PRL release. BW755c or RHC 80267, both of which reduce the production of arachidonic acid metabolites, including 5-HETE, significantly reduced basal PRL release. The inhibitory effects of BW755c and RHC 80267 on PRL release, however, could be overcome by the addition of 5- HETE.

In conclusion, 5-HETE or similar lipoxygenase metabolites may be important cellular components in the process of PRL release, and the inhibitory action of dopamine on PRL would seem to be mediated at some step after stimulation by these metabolites. (Endocrinology 116: 1813–1817, 1985)

Footnotes

^* Supported by USPHS Grant CA-07535 (to R.M.M.) and USPHS Fellowship F-32-CA07137 (to A.J.M).

To whom requests for reprints should be addressed.

Received August 7, 1984.