Effects of prostaglandin E2 on the electrical property of the pregnant mouse myometrium.

At any stage of gestation, low concentrations of PGE2 increased that frequency and number of spikes in a train discharge without any marked change of the membrane potential. An increased concentration depolarized the membrane and produced continuous spike generation. A further increase in concentration of PGE2 produced a depolarization block of spike generation. The sensitivity of the myometrium to PGE2 was markedly increased during the progress of gestation so that at the late stage of gestation, the sensitivity was more than 100 times greater than at the early stage. The longitudinal muscle showed a higher sensitivity to PGE2 than the circular muscle. However, both muscles showed a similar sensitivity to oxytocin. In the longitudinal muscle, desensitization to PGE2 occurred more quickly than to oxytocin. When PGE2 produced a slight depolarization of the membrane, the membrane resistance was increased. However, when the membrane potential was displaced to the control level by applying a hyperpolarizing current, the membrane resistance was slightly reduced. Displacement of the membrane potential to the level before drug application restored spike generation. However, the membrane resistance was still reduced. In Na-deficient Locke solution or in Ca-free Mg-Locke solution, the depolarization induced by PGE2 was suppressed but not suppressed by, in K-deficient Locke solution.