The roles of nitric oxide and prostaglandins in myometrium at proterm

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We demonstrated that an L-arginine-NOL-cGMP pathway exists in pregnant rat uterus, through in vitro and in vivo experiments. Nitric oxide inhibits spontaneous contractions in rat uterus at midgestation but not at term, demonstrating gestational age-dependent inhibition. The presence of placental tissue enhances inhibition of uterine contractility by agents that spontaneously release nitric oxide, such as diethylamine-nitric oxide, but not by nitroglycerin, which requires metabolic transformation for nitric oxide to be released. Refractoriness to nitric oxide near or at term does not depend on the presence or absence of placental tissue.The plasma NO metabolite concentration in 22-26 weeks of pregnancy was significantly higher than that of the non pregnant women, although the plasma NO nietabolite concentration was slightly decreased toward term. The plasma NO metabolite concentration in patients with preterm labor was lower than that of the normal pregnant women in same weeks of pregnancy.These studies suggest that NO has an important role in maintaining uterine quiescence at midgestation. A decrease in uterine relaxation responsiveness to NO at term may play a role in the initiation of labor. Furthermore, LPS attenuated the inhibition of contraction by NO. Myometrium with infection at midgestation seems to increase sensitivity to contractility compared to normal myometrium at late gestation. Effect of placental factor which is attenuated on inhibition of contractions by NO did not depend on iNOS in uterus Chorioaminionitis might induce preterm labor via an iNOS-independent mechanism.