Brunetti L, Ragazzoni E, Preziosi P, Vacca M
Department of Pharmacology, G. D'Annunzio University, Chieti, Italy.
Life Sci. 1995 Mar 3;56(15):PL277-83. doi: 10.1016/0024-3205(95)00077-1.
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.
在先前的实验中我们已经表明，一氧化氮（NO）能够在体外调节培养的大鼠下丘脑和垂体前叶细胞释放促肾上腺皮质激素释放激素（CRH）和促肾上腺皮质激素（ACTH）。现在，我们展示了NO参与基础和白细胞介素-1β诱导的催乳素（PRL）释放的实验证据。一氧化氮合酶抑制剂L-NG-硝基精氨酸和NO清除剂血红蛋白损害基础和白细胞介素-1β诱导的PRL释放，而NO供体吗多明能够释放PRL并放大白细胞介素-1β诱导的PRL释放，证实了一氧化氮在垂体激素分泌中的调节作用。另一方面，我们的实验没有得出关于前列腺素E2（PGE2）在白细胞介素-1β诱导的PRL释放中可能作用的证据。
