Nanjo T
Br J Pharmacol. 1984 Mar;81(3):427-40. doi: 10.1111/j.1476-5381.1984.tb10095.x.
Effects of acetylcholine (ACh) and noradrenaline (NA) on mechanical properties of smooth muscle cells of the guinea-pig portal vein were investigated using intact and skinned muscle preparations. In some preparations, the electrical activity was also recorded. In addition to ACh and NA, the effects of caffeine, procaine, excess concentrations of [K]o and MnCl2 were investigated. NA enhanced the mechanical response due to increase in the spike generation, receptor activated depolarization and release of Ca stored in the cell. ACh also enhanced the mechanical response, but this agent had little effect on the Ca release from the storage sites. Caffeine and procaine (10 mM) depolarized the membrane and enhanced the electrical activity. Caffeine enhanced the mechanical activity due to an increase in the membrane activity and the release of Ca stored in the cell, while procaine inhibited the contraction. Procaine inhibited and caffeine accelerated the Ca-induced Ca-release mechanism in the cell. NA released the Ca from the storage sites to a greater extent than did caffeine or ACh. MnCl2 inhibited the spontaneous membrane activity and contraction; however, low concentrations of MnCl2 increased the caffeine- or NA-induced contraction in Ca-free solution. When the Ca-tension relationship was observed in saponin-treated skinned muscles, the minimum concentration of Ca required to produce the contraction was 10(-7)M, as observed in other vascular tissues. Caffeine released the stored Ca, Na and ACh had no effect on the Ca release and procaine inhibited the caffeine-induced Ca release in skinned muscles. It was concluded that the membrane properties of smooth muscle cells in the portal vein are much the same as observed in other spontaneously active visceral muscles. Differences observed in the actions of NA and ACh on mechanical properties seems to be mainly due to different receptor-operated Ca release mechanisms.
采用完整和去膜的肌肉标本，研究了乙酰胆碱（ACh）和去甲肾上腺素（NA）对豚鼠门静脉平滑肌细胞力学特性的影响。在一些标本中，还记录了电活动。除ACh和NA外，还研究了咖啡因、普鲁卡因、高浓度的细胞外钾离子（[K]o）和氯化锰（MnCl2）的作用。NA由于动作电位产生增加、受体激活的去极化以及细胞内储存钙的释放，增强了力学反应。ACh也增强了力学反应，但该药物对储存部位的钙释放影响很小。咖啡因和普鲁卡因（10 mM）使膜去极化并增强了电活动。咖啡因由于膜活性增加和细胞内储存钙的释放而增强了力学活性，而普鲁卡因则抑制收缩。普鲁卡因抑制而咖啡因加速细胞内钙诱导的钙释放机制。NA比咖啡因或ACh更能从储存部位释放钙。MnCl2抑制自发的膜活性和收缩；然而，低浓度的MnCl2在无钙溶液中增加了咖啡因或NA诱导的收缩。当在皂素处理的去膜肌肉中观察钙-张力关系时，产生收缩所需的最低钙浓度为10^(-7)M，这与其他血管组织中观察到的情况相同。咖啡因释放储存的钙，Na和ACh对钙释放无影响，普鲁卡因抑制去膜肌肉中咖啡因诱导的钙释放。得出的结论是，门静脉平滑肌细胞的膜特性与其他自发活动的内脏肌肉中观察到的情况非常相似。NA和ACh对力学特性作用的差异似乎主要归因于不同的受体介导的钙释放机制。
