Effects of nitric oxide and carbon monoxide on CRH secretion from cultured placental trophoblasts

Humanplacentasecreteslargeamountsofhypothalamichormone,corticotropin--releasinghormone(CRH))intobothmaternalandfetalcirculationduringpregnancy.MaternalplasmaCRHrisesfrommidgestationtotermandpeakatlaborinpregantwomen.TheplacentalsyncytiotrophoblastcontainingbothCRHpeptideanditsgeneislikelytobethemajorsourceofthiscirculatingCRH.PlacentalCRHhasrecentlybeenlinkedtoplacentalclockdetermininggestationallengthandtobeatriggerofhumanlaborlj.Inaddition,abnormallyelevatedCRHconcentrationsinmatern…

Effects of nitric oxide and carbon monoxide on CRH secretion from cultured placental trophoblasts

To investigate the effects of nitric oxide (NO) and carbon monoxide (CO) on corticotropin releasing hormone (CRH) secretion from cultured placental cells. Methods: Changes of CRH contents in culture media were observed after cultured placental cells were treated with NO and CO donors or precursors, NO synthase (NOS) and heme oxygenase (HO) inhibitors and guanylate cyclase inhibitor respectively. Measurement of CRH contents was performed by radioimmunoassay (RIA). Results: Sodium nitroprusside (SNP), NO donor, inhibited hasal and KCl stimulated CRH secretion from cultured placental cells.This effect could be reversed by L-nitro-arginie methyl ester (L-NAME), a NOS inhibitor. L-NAME also increased hasal CRH secretion. LY83583, a guanylate cyclase inhibitor, reversed SNP-induced suppression of CRH secretion and enhanced basal CRH secretion. However, CO precursor Hemin and HO inhibitor ZnPP9,did not affect basal and KCl-stimulated CRH secretion. Conclusion: Exogenous and endogenous NO could inhibit CRH secretion from placental cells. CO has no effect on CRH secretion from placental cells. The inhibitory effect of NO on CRH exocytosis is mediated by cGMP.