抄録
Ovariectomized rats were given one-shot injections of 10μg estradiol-17β benzoate, and the longitudinal muscle of the uterus was used for experiment 4 days later. The membrane potential was 58.8± 2.4mV, and the membrane activity consisted of repetitive spike potentials carried on a plateau potential. Oxytocin (1mU/ml) caused a depolarization of 7.6±3.7mV in a Mg-free Locke solution, a prolongation of burst discharge and increase in the frequency of spontaneous activity. The effects were potentiated by 1-3mM Mg. Burst discharge was abol-ished by the application of 0.5mM Mn, and resumed when 0.1mU/ml oxytocin was applied. Depolarization up to about -30mV and a con-tracture were caused by 1mU oxytocin when applied with 1-2mM Mn. The excitatory effect of oxytocin was depressed by 5mM Mn. Marked depolarization and contracture were produced by 1 mU oxytocin when the application of Mn was discontinued (rebound phenomenon). The above observations indicate the superficial site of Mg and Mn at low concentration in cooperative action with oxytocin, and an additional site of Mn for the rebound potentiation of contraction and depolariza-tion. It is proposed that oxytocin accelerated Mn influx, and that intra-cellular Mn participates in electrical and contractile responses due to the application of oxytocin. In this respect, acetylcholine caused a similar effect.
