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

以豚鼠胃为实验材料，研究了平滑肌自发活动产生的细胞机制。由于缝隙连接的分析对于理解起搏非常重要，因此使用微血管对缝隙连接进行了实验。胃肌由环状、纵向和间质细胞组成，每种细胞产生不同的电活动模式。环行肌的准备显示出瞬时的去极化，这些去极化加在一起形成了一个巨大的再生潜力。去极化脉冲诱发再生电位的延迟时间较长(约1 S)，再生电位表现出较长的不应期(15~20 S)。BAPTA使细胞内钙离子减少或CPA破坏SR的功能使再生潜能消失。硝苯地平不影响这些反应。我们推测再生潜能的产生与不明渠道有关。18-β-甘草次酸(GA)使内皮与平滑肌之间的电连接解离，使乙酰胆碱引起的超极化消失，提示内皮依赖性超极化可能是内皮细胞通过缝隙连接产生的电信号。结果表明，在不考虑体液物质的情况下，可以解释EDHF诱发的超极化现象。

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.