Hashitani H, Fukuta H, Takano H, Klemm M F, Suzuki H
Department of Physiology, Nagoya City University Medical School, Mizuho-Ku, Nagoya 467-8601, Japan.
J Physiol. 2001 Jan 15;530(Pt 2):273-86. doi: 10.1111/j.1469-7793.2001.0273l.x.
The origin and propagation of waves of spontaneous excitation in bundles of smooth muscle of the guinea-pig bladder were examined using intracellular recording techniques and visualization of the changes in the intracellular calcium concentration ([Ca2+]i). Bladder smooth muscle cells exhibited spontaneous transient increases in [Ca2+]i which originated along a boundary of each smooth muscle bundle and then spread to the other boundary with a conduction velocity of 2.0 1r1r>mm1> s-1. Spontaneous increases in [Ca2+]i were always preceded by action potentials. Nifedipine (10 microM) abolished increases in both [Ca2+]i and action potentials. Caffeine (10 1s1sFmM1F), ryanodine (50 microM) and cyclopiazonic acid (10 microM reduced the amplitude of the associated increases in [Ca2+]i without preventing the generation of action potentials. Spontaneous action potentials had conduction velocities of 40 1t1t>mm 1> s-1 in the axial direction and 1.3 1u1u>mm 1> s-1 in the transverse direction. The electrical length constants of the bundles of muscle were 425 microM in the axial direction and 12.5 microM in the transverse direction. Neurobiotin, injected into an impaled smooth muscle cell, spread more readily to neighbouring cells located in the axial direction than those located in the transverse direction. The spread of neurobiotin was inhibited by 18beta-glycyrrhetinic acid (18beta-GA, 40 microM), a gap junction blocker. Immunohistochemistry for Connexin 43 showed abundant punctate staining on the smooth muscle cell membranes. These results suggested that spontaneous action potentials and associated calcium waves occur almost simultaneously along the boundary of bladder smooth muscle bundles and then propagate to the other boundary probably through gap junctions.
利用细胞内记录技术以及细胞内钙浓度（[Ca2+]i）变化的可视化技术，对豚鼠膀胱平滑肌束中自发兴奋波的起源和传播进行了研究。膀胱平滑肌细胞表现出[Ca2+]i的自发瞬时升高，其起源于每个平滑肌束的边界，然后以2.0mm/s的传导速度传播至另一边界。[Ca2+]i的自发升高总是先于动作电位出现。硝苯地平（10μM）可消除[Ca2+]i和动作电位的升高。咖啡因（10mM）、ryanodine（50μM）和环匹阿尼酸（10μM）可降低相关的[Ca2+]i升高幅度，但不阻止动作电位的产生。自发动作电位在轴向的传导速度为40mm/s，在横向的传导速度为1.3mm/s。肌肉束的电长度常数在轴向为425μM，在横向为12.5μM。注入刺入的平滑肌细胞中的神经生物素，向轴向相邻细胞的扩散比向横向相邻细胞的扩散更容易。神经生物素的扩散受到缝隙连接阻滞剂18β-甘草次酸（18β-GA，40μM）的抑制。连接蛋白43的免疫组织化学显示在平滑肌细胞膜上有丰富的点状染色。这些结果表明，自发动作电位和相关的钙波几乎同时沿着膀胱平滑肌束的边界出现，然后可能通过缝隙连接传播至另一边界。
