Modification by magnesium and manganese ions of the effects of oxytocin on the electrical and mechanical activity of the longitudinal muscle of estrogen-treated rat uterus.

Ovariectomized rats were given one-shot injections of 10 microgram estradiol-17 beta benzoate, and the longitudinal muscle of the uterus was used for experiment 4 days later. The membrane potential was 58.8 +/- 2.4 mV, and the membrane activity consisted of repetitive spike potentials carried on a plateau potential. Oxytocin (1 mU/ml) caused a depolarization of 7.6 +/- 3.7 mV in a Mg-free Locke solution, a prolongation of burst discharge and increase in the frequency of spontaneous activity. The effects were potentiated by 1-3 mM Mg. Burst discharge was abolished by the application of 0.5 mM Mn, and resumed when 0.1 mU/ml oxytocin was applied. Depolarization up to about - 30 mV and a contracture were caused by 1 mU oxytocin when applied with 1-2 mM Mn. The excitatory effect of oxytocin was depressed by 5 mM 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 depolarization. It is proposed that oxytocin accelerated Mn influx, and that intracellular Mn participates in electrical and contractile responses due to the application of oxytocin. In this respect, acetylcholine caused a similar effect.