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首页> 美国卫生研究院文献>The Journal of Physiology >Role of interstitial cells and gap junctions in the transmission of spontaneous Ca2+ signals in detrusor smooth muscles of the guinea-pig urinary bladder
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Role of interstitial cells and gap junctions in the transmission of spontaneous Ca2+ signals in detrusor smooth muscles of the guinea-pig urinary bladder

机译：间质细胞和间隙连接在豚鼠膀胱逼尿肌平滑肌自发Ca2 +信号传递中的作用

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摘要

To investigate mechanisms underlying the transmission of spontaneous Ca2+ signals in the bladder, changes in intracellular concentrations of Ca2+ ([Ca2+]i) were visualized in isolated detrusor smooth muscle bundles of the guinea-pig urinary bladder loaded with a fluorescent Ca2+ indicator, fura-PE3 or fluo-4. Spontaneous increases in [Ca2+]i (Ca2+ transients) preferentially originated along the boundary of muscle bundles and then spread to the other boundary (Ca2+ waves). The synchronicity of Ca2+ waves across the bundles was disrupted by 18β-glycyrrhetinic acid (18β-GA, 40 μm), carbenoxolone (30 μm) or 2-aminoethoxydiphenylborate (2-APB, 50–100 μm), while CPA (10 μm), ryanodine (100 μm), xestospongin C (3 μm) and U-73122 (10 μm) had no effect. Intracellular recordings using two independent microelectrodes demonstrated that 2-APB (100 μm) blocked electrical coupling between detrusor smooth muscle cells. Nifedipine (10 μm) but not nominal Ca2+-free solution diminished the synchronicity of Ca2+ waves before preventing their generation. Staining for c-kit identified interstitial cells (IC) located along both boundaries of muscle bundles. IC were also scattered amongst smooth muscle cells and were more dominantly distributed in connective tissue between muscle bundles. IC generated nifedipine-resistant spontaneous Ca2+ transients, which occurred independently of those of smooth muscles. In conclusion, the propagation of Ca2+ transients in the bladder appears to be exclusively mediated by the spread of action potentials through gap junctions being facilitated by the regenerative nature of L-type Ca2+ channels, without significant contribution of intracellular Ca2+ stores. IC in the bladder may modulate the transmission of Ca2+ transients originating from smooth muscle cells rather than being the pacemaker of spontaneous activity.
机译：为了研究自发Ca 2 + 信号在膀胱中传递的基础机制，细胞内Ca 2 + （[Ca 2 + ] i）在装有荧光Ca 2 + 指示剂，fura-PE3或fluo-4的豚鼠膀胱的逼尿肌平滑肌束中可视化。 [Ca 2 + ] i（Ca 2 + 瞬态）的自发增加优先起源于肌肉束的边界，然后扩展到另一个边界（Ca 2 + 波）。束中Ca 2 + 的同步性被18β-甘草次酸（18β-GA，40μm），羧苄酮（30μm）或2-氨基乙氧基二苯基硼酸酯（2-APB，50-100）破坏。 μm），而CPA（10μm），ryanodine（100μm），xestospongin C（3μm）和U-73122（10μm）无效。使用两个独立的微电极进行的细胞内记录表明，2-APB（100μm）阻断了逼尿肌平滑肌细胞之间的电耦合。硝苯地平（10μm），但没有标称的不含Ca 2 + 的溶液，在防止其生成之前会减弱Ca 2 + 的同步性。沿肌束两个边界染色的c-kit识别的间质细胞（IC）染色。 IC也散布在平滑肌细胞中，并且更主要地分布在肌束之间的结缔组织中。 IC产生耐硝苯地平的自发Ca 2 + 瞬变，其发生与平滑肌无关。总之，Ca 2 + 瞬变在膀胱中的传播似乎完全是由L型Ca 2+的再生性质促进了通过间隙连接的动作电位的传播所介导的。 通道，对细胞内Ca 2 + 存储没有显着贡献。膀胱中的IC可能调节源自平滑肌细胞的Ca 2 + 瞬变的传递，而不是自发活动的起搏器。

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