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目的：研究一氧化氮（ＮＯ）和一氧化碳（ＣＯ）及其细胞内信使ｃＧＭＰ对培养的胎盘细胞促肾上腺皮质素释放素（ＣＲＨ）分泌的调节作用。方法：采用细胞培养技术观察体外培养的胎盘细胞分别给予ＮＯ和ＣＯ的供体或前体、ＮＯ合酶和血红素加氧酶的抑制剂以及鸟苷酸环化酶的抑制剂后，培养上清和细胞内ＣＲＨ含量的变化。ＣＲＨ含量的测定应用放射免疫分析技术。结果：ＮＯ供体硝普钠不仅可显著抑制ＣＲＨ的基础分泌，还可抑制由ＫＣｌ刺激所致的ＣＲＨ的释放。ＮＯ合酶的抑制剂Ｌ－硝基－精氨酸甲酯和鸟苷酸环化酶抑制剂ＬＹ８３５８３可逆转硝普钠对ＣＲＨ分泌的抑制作用，还可促进ＣＲＨ的基础分泌。ＣＯ前体Ｈｅｍｉｎ和血红素加氧酶的抑制剂ＺｎＰＰ９对ＣＲＨ的基础分泌和ＫＣｌ刺激引起的ＣＲＨ的释放均无影响。结论：外源性和内源性的ＮＯ均可抑制胎盘ＣＲＨ的分泌。ＮＯ抑制胎盘ＣＲＨ分泌的作用可能是由ｃＧＭＰ介导的。ＣＯ对胎盘ＣＲＨ的分泌无影响
AIM: To investigate the regulatory effect of nitric oxide (NO) and carbon monoxide (CO) and their intracellular messenger cGMP on the secretion of corticotropin-releasing hormone (CRH) in cultured placental cells. Methods: The cell culture technique was used to observe the effects of NO and CO donor or precursor, NO synthase inhibitor, heme oxygenase inhibitor and guanylate cyclase inhibitor on placental cells cultured in vitro. Qing and intracellular CRH content changes. CRH content determination using radioimmunoassay technology. RESULTS: NO donor sodium nitroprusside not only significantly inhibited the basal secretion of CRH, but also inhibited the release of CRH induced by KCl stimulation. The inhibitor of NO synthase, L-nitro-arginine methyl ester and guanylate cyclase inhibitor LY83583, reverses the inhibitory effect of sodium nitroprusside on CRH secretion and promotes basal secretion of CRH. CO precursor Hemin and heme oxygenase inhibitor ZnPP9 had no effect on the basal secretion of CRH and the release of CRH by KCl stimulation. Conclusion: Exogenous and endogenous NO can inhibit the secretion of CRH in the placenta. The effect of NO on placental CRH secretion may be mediated by cGMP. CO has no effect on the secretion of placental CRH