The role of nitric oxide on uterine contraction at preterm

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We demonstrated that an L-arginine-NO-cGMP pathway exists in pregnant rat uterus, through in vitro and in vivo experiments. Nitric oxide inhibits spontaneous contractions in rate uterus at midgestation but not at term, demonstrating gestational age-dependent inhibition. There is gestational age-dependent refractoriness to calcium-dependent potassium but not adenosine triphosphate-dependent potassium channel opener-induced inhibition of spontaneous contractile activity of isolated rat uterine rings. Nitric oxide inhibits uterine contractions by opening of calcium-dependent potassium channels in pregnant rat myometrium. Refractoriness to nitric oxide toward term may result from decreased probability to open or number of calcium-dependent potassium channels. The presence of placental tissue enhances inhibition of uterine contractility by agents that spontaneously release nitric oxide, such as diethylamine-nitric oxide, but no 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 metabolite 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. Therefore, decreasing NO products may be one of the causes of preterm birth.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. Nitric oxide donor drugs may be very effective in suppressing preterm labor.