Physiological studies of the cellular mechanisms of the generation of spontaneous activity in smooth muscle

用豚鼠胃研究了平滑肌自发活动产生的细胞机制。由于缝隙连接的研究对于理解心脏起搏机制具有重要意义，本研究利用微血管对缝隙连接进行了实验研究。胃肌由环形细胞、纵行细胞和间质细胞组成，每种细胞产生不同的电活动模式。环形肌肉制备显示短暂去极化，其加在一起形成大的再生潜力。去极化脉冲诱发的再生电位延迟时间较长（约1 s），呈长不应期（15-20 s）。BAPTA引起的细胞内Ca ~（2+）减少或CPA引起的SR功能障碍均使再生电位消失。这些反应不受硝苯地平。我们推测参与的未知渠道的再生潜力的产生。18-β葡萄糖大黄酸（GA）使血管内皮细胞与平滑肌细胞之间的电连接断开，乙酰胆碱引起的平滑肌细胞超极化消失，提示血管内皮细胞通过缝隙连接产生内皮依赖性超极化。结果表明，它是可能的解释EDHF引起的超极化，而不考虑体液物质。

The cellular mechanisms of generation of spontaneous activity in smooth muscle were investigated using the guinea-pig stomach. As the analysis of gap junction is important for understanding the pacemaking, experiments were carried out on gap junctions using microvessels.Gastric muscles consisted of circular, longitudinal and interstitial cells, and each produced different patterns of electrical activity. The circular muscle preparation revealed transient depolarization which summed together to form a large regenerative potential. Depolarizing pulse evoked the regenerative potential with long delay (about 1 s), and the potential showed long refractoxy periods (15-20 s). Reduction of intracellular Ca ions by BAPTA or disfunction of SR by CPA abolished the regenerative potential. These responses were not affected by nifedipine. We speculate an involvement of unidentified channel for generation of the regenerative potential. Ca ions from SR were considered important.Dissociation of electrical connections between endothelium and smooth muscle by 18-beta glycirrhetinic acid (GA) caused disappearance of acetylcholine-induced hyperpolarization in smooth muscle, and the results suggested that endothelium-dependent hyperpolarization may be produced an electrical signal from endothelium through gap junctions. The results indicated that it is possible to explain the EDHF-induced hyperpolarization without considering a humoral substance.