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首页> 美国卫生研究院文献>Biophysical Journal >Pacemaking through Ca2+ Stores Interacting as Coupled Oscillators via Membrane Depolarization
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Pacemaking through Ca2+ Stores Interacting as Coupled Oscillators via Membrane Depolarization

机译：通过Ca2 +进行起搏通过膜去极化作为耦合的振荡器相互作用

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This study presents an investigation of pacemaker mechanisms underlying lymphatic vasomotion. We tested the hypothesis that active inositol 1,4,5-trisphosphate receptor (IP3R)-operated Ca2+ stores interact as coupled oscillators to produce near-synchronous Ca2+ release events and associated pacemaker potentials, this driving action potentials and constrictions of lymphatic smooth muscle. Application of endothelin 1 (ET-1), an agonist known to enhance synthesis of IP3, to quiescent lymphatic smooth muscle syncytia first enhanced spontaneous Ca2+ transients and/or intracellular Ca2+ waves. Larger near-synchronous Ca2+ transients then occurred leading to global synchronous Ca2+ transients associated with action potentials and resultant vasomotion. In contrast, blockade of L-type Ca2+ channels with nifedipine prevented ET-1 from inducing near-synchronous Ca2+ transients and resultant action potentials, leaving only asynchronous Ca2+ transients and local Ca2+ waves. These data were well simulated by a model of lymphatic smooth muscle with: 1), oscillatory Ca2+ release from IP3R-operated Ca2+ stores, which causes depolarization; 2), L-type Ca2+ channels; and 3), gap junctions between cells. Stimulation of the stores caused global pacemaker activity through coupled oscillator-based entrainment of the stores. Membrane potential changes and positive feedback by L-type Ca2+ channels to produce more store activity were fundamental to this process providing long-range electrochemical coupling between the Ca2+ store oscillators. We conclude that lymphatic pacemaking is mediated by coupled oscillator-based interactions between active Ca2+ stores. These are weakly coupled by inter- and intracellular diffusion of store activators and strongly coupled by membrane potential. Ca2+ store-based pacemaking is predicted for cellular systems where: 1), oscillatory Ca2+ release induces depolarization; 2), membrane depolarization provides positive feedback to induce further store Ca2+ release; and 3), cells are interconnected. These conditions are met in a surprisingly large number of cellular systems including gastrointestinal, lymphatic, urethral, and vascular tissues, and in heart pacemaker cells.
机译：这项研究提出了对淋巴管血管运动起搏器机制的调查。我们测试了一种假设，即活性肌醇1,4,5-三磷酸受体（IP3R）操作的Ca 2 + 存储作为耦合振荡器相互作用，产生接近同步的Ca 2 + 释放事件和相关的起搏器电位，这种驱动动作电位和淋巴平滑肌收缩。将内皮素1（ET-1）（一种已知可增强IP3合成的激动剂）应用于静止的淋巴平滑肌合胞体，首先可增强自发Ca 2 + 瞬变和/或细胞内Ca 2+ < / sup>挥手。然后发生较大的近同步Ca 2 + 瞬变，从而导致与动作电位和随之产生的血管运动相关的全局同步Ca 2 + 瞬变。相反，用硝苯地平阻断L型Ca 2 + 通道可阻止ET-1诱导近同步的Ca 2 + 瞬变和由此产生的动作电位，仅留下异步的Ca 2 + 瞬变和局部Ca 2 + 波。这些数据通过具有以下特征的淋巴平滑肌模型得到了很好的模拟：1）IP3R操纵的Ca 2 + 存储区中的振荡Ca 2 + 释放，导致去极化； 2），L型Ca 2 + 通道； 3）细胞之间的间隙连接。商店的刺激通过耦合的基于商店的振荡带动了全球起搏器活动。膜电位变化和L型Ca 2 + 通道产生更多存储活性的正反馈是该过程的基础，它提供了Ca 2 + 存储之间的长期电化学耦合振荡器。我们得出结论，淋巴节律起搏是由活跃的Ca 2 + 商店之间基于耦合的振荡器相互作用介导的。这些通过商店激活剂的细胞间和细胞内扩散而弱耦合，并通过膜电位而强烈耦合。预测基于Ca 2 + 存储的起搏对于蜂窝系统而言如下：1）振荡的Ca 2 + 释放引起去极化； 2），膜去极化提供正反馈，以诱导进一步储存Ca 2 + 的释放；和3），单元相互连接。这些条件在包括胃肠道，淋巴，尿道和血管组织在内的大量细胞系统以及心脏起搏器细胞中得到了满足。

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