In previous experiments we have shown that nitric oxide (NO) was able to modulate CRH and ACTH release from cultured rat hypothalamic and anterior pituitary cells, in vitro. Now, we show experimental evidence of an involvement of NO in basal and interleukin-1 beta-induced prolactin (PRL) release. L-NG-nitro-arginine, an inhibitor of nitric oxide synthetase, and hemoglobin, a NO scavenger, impaired basal and interleukin-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 secretion. On the other hand, no evidence regarding a possible role of prostaglandin E2 (PGE2) in IL-1beta-induced PRL release came out from our experiments.