Inoue Y, Shimamura K, Sperelakis N
Department of Physiology and Biophysics, College of Medicine, University of Cincinnati, Ohio 45267-0576.
Can J Physiol Pharmacol. 1992 Dec;70(12):1597-603. doi: 10.1139/y92-229.
The effects of oxytocin, a uterotonic polypeptide hormone, on the voltage-dependent slow calcium, fast sodium, and potassium channel currents were studied using whole-cell voltage clamp of freshly isolated cells from late pregnant (18-21 day) rat myometrium. The calcium current was rapidly inhibited by oxytocin (about 25% inhibition at 20 nM) in a dose-dependent manner, and this inhibitory effect was completely reversible by washout. However, inhibition was not observed when barium was used as the charge carrier. Sodium current and potassium current were not modified by oxytocin, thus sodium and potassium currents may not play important roles in oxytocin-induced augmentation of uterine contraction. It is concluded that oxytocin stimulates uterine contraction by mechanisms other than augmentation of the voltage-dependent calcium current, e.g., by release of Ca from sarcoplasmic reticulum (by inositol triphosphate) or by activation of a receptor-operated Ca channel. The inhibition of the slow calcium current may be induced by the elevation of [Ca]i.
使用全细胞膜片钳技术，对来自妊娠晚期（18 - 21天）大鼠子宫肌层的新鲜分离细胞进行研究，以探讨子宫收缩多肽激素催产素对电压依赖性慢钙通道、快钠通道和钾通道电流的影响。催产素能迅速抑制钙电流（20 nM时约有25%的抑制率），且呈剂量依赖性，这种抑制作用经洗脱后可完全逆转。然而，当使用钡作为载流子时，未观察到抑制作用。催产素对钠电流和钾电流无影响，因此钠电流和钾电流可能在催产素诱导的子宫收缩增强中不起重要作用。研究得出结论，催产素通过电压依赖性钙电流增强以外的机制刺激子宫收缩，例如通过肌醇三磷酸从肌浆网释放钙或通过激活受体操纵性钙通道。慢钙电流的抑制可能是由细胞内钙浓度升高引起的。
