Role of Arachidonate Metabolism on the in vitro Release of Luteinizing Hormone and Prolactin from the Anterior Pituitary Gland: Possible Involvement of Lipoxygenase Pathway

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Abstract
The aim of the present study was to evaluate whether arachidonic acid metabolism may play a role on luteinizing hormone (LH) and prolactin (PRL) release directly at the pituitary level. To this purpose, exogenous arachidonic acid, alone or in presence of inhibitors of cycloxygenase (indomethacin:IND) and lipoxygenase pathways (nordihydroguaiaretic acid:NDGA), was added to perfused rat anterior pituitary cells. PGE, PGFα, LH and PRL levels present in the eluate were assayed with specific RIA methods. Both PGE and PGFα show a dose-related response after the addition of increasing doses of arachidonic acid. The addition of 0.05 mM arachidonic acid induces an increase of LH and PRL. The addition of IND to the perfusion medium highly potentiates the stimulatory effects induced by arachidonic acid on LH and PRL release. On the contrary, the addition to the medium of either NDGA or IND plus NDGA completely reverses the stimulatory action induced by arachidonic acid alone. The present results suggest that: (1) adenohypophyseal cells are able to metabolize exogenous arachidonic acid; (2) arachidonic acid induces an elevation in LH and PRL levels; (3) lipoxygenase pathway metabolite(s) are likely involved in these activities, and (4) the site of action of arachidonic acid is at the pituitary level.

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