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

利用豚鼠胃研究了平滑肌自发活动产生的细胞机制。由于对间隙连接的分析对理解起搏器起搏有重要意义，我们利用微血管对间隙连接进行了实验。胃肌肉由圆形细胞、纵向细胞和间质细胞组成，每个细胞产生不同的电活动模式。圆形肌肉制备显示出短暂的去极化，这些因素综合起来形成了巨大的再生潜力。去极化脉冲诱发再生电位的时间延迟较长（约1 s），而再生电位的折射周期较长（15 ~ 20 s）。BAPTA对细胞内Ca离子的减少或CPA对SR功能的破坏使再生潜能消失。硝苯地平对这些反应没有影响。我们推测再生潜能的产生涉及一个未知的渠道。锶中的钙离子被认为是重要的。18- β -甘次酸（GA）解离内皮与平滑肌之间的电连接，使乙酰胆碱诱导的平滑肌超极化消失，提示内皮依赖性超极化可能通过间隙连接从内皮产生电信号。结果表明，在不考虑体液物质的情况下，可以解释edhf诱导的超极化。

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.