A POSSIBLE ROLE FOR NITRIC-OXIDE BUT NOT FOR PROSTAGLANDIN E(2) IN BASAL AND INTERLEUKIN-1-BETA-INDUCED PRL RELEASE IN-VITRO

In previous experiments we have shown that nitric oxide (NO) was able to modulate CRH and ACTH release from cultured rat hypothalamic and an terior pituitary cells, in vitro. Now, we show experimental evidence o f an involvement of NO in basal and interleukin-1 beta-induced prolact in (PRL) release. L-N-G-nitroarginine, an inhibitor of nitric oxide sy nthetase, and hemoglobin, a NO scavenger, impaired basal and interleuk in-1-beta-induced PRL release, while molsidomine, a NO donor, was able to release PRL and to amplify interleukin-1-beta-induced PRL release, confirming a modulatory role for nitric oxide in pituitary hormone se cretion. On the other hand, no evidence regarding a possible role of p rostaglandin E(2) (PGE(2)) in IL-1 beta-induced PRL release came out f rom our experiments.