A mathematical model of electrophysiological activity in a bullfrog atrial cell.
A mathematical model of electrophysiological activity in a bullfrog atrial cell.
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牛蛙心房细胞电生理活动的数学模型。
DOI：
10.1152/ajpheart.1990.259.2.h370
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Campbell,DL
中科院分区：
文献类型：
--
作者：
Rasmusson,RL;Clark,JW;Giles,WR;Robinson,K;Clark,RB;Shibata,EF;Campbell,DL
我们已经开发了一个模型，心脏心房电活动的基础上获得的电压钳测量从牛蛙心房分离的单细胞。这些测量使我们能够模拟一些被认为是重要的动作电位启动，复极，和兴奋收缩（EC）耦合过程中的过程。在该心房模型中，细胞膜包含通道介导的（Na+、Ca 2+、内向整流K+、延迟整流K+、线性背景泄漏）和转运蛋白介导的（Na（+）-K+泵、Na（+）-Ca 2+交换器、Ca 2+泵）电流。细胞外被扩散受限空间包围。细胞内容积含有Ca 2（+）结合蛋白（钙调蛋白、肌钙蛋白）。该模型做出了几个重要的预测。1)Ca 2+电流的不完全失活提供了向内电流，维持了动作电位的平台期。2)延迟整流钾电流的激活启动复极。3)由于肌浆蛋白对Ca ~（2+）的缓冲作用，Na ~（+）-Ca ~（2+）交换电流较小，对复极影响不大。4)Na（+）-K+泵电流在复极化中不起主要作用。5)K+积累和Ca ~（2+）耗竭可能发生在细胞外间隙。6)EC偶联的调节由肌浆Ca 2（+）结合蛋白之间的相互作用控制;具体而言，变力性“正阶梯效应”可以通过肌钙蛋白上竞争性结合位点处Ca 2+和Mg 2+之间的相互作用来解释。当结合我们的静脉窦中主要起搏模型的结果考虑时[Rasmusson等人，Am. J. Physiol.259（Heart Circ.生理学28）：H352-H369，1990]，该心房模型显示了某些跨膜电流的存在或不存在如何改变动作电位特性，并因此改变各种转运蛋白介导的和通道介导的电流的相对影响。
We have developed a model of cardiac atrial electrical activity based on voltage-clamp measurements obtained from single cells isolated from the bullfrog atrium. These measurements have allowed us to simulate a number of processes thought to be important in action potential initiation, repolarization, and the excitation-contraction (EC) coupling process. In this atrial model, the cell membrane contains both channel-mediated (Na+, Ca2+, inward rectifier K+, delayed rectifier K+, linear background leak) and transporter-mediated (Na(+)-K+ pump, Na(+)-Ca2+ exchanger, Ca2+ pump) currents. The cell is surrounded extracellularly by a diffusion-limited space. The intracellular volume contains Ca2(+)-binding proteins (calmodulin, troponin). The model makes several important predictions. 1) Incomplete inactivation of the Ca2+ current provides an inward current the maintains the plateau of the action potential. 2) Activation of the delayed rectifier K+ current initiates repolarization. 3) Due to Ca2+ buffering by myoplasmic proteins the Na(+)-Ca2+ exchanger current is relatively small and has little influence on repolarization. 4) The Na(+)-K+ pump current does not play a major role in repolarization. 5) K+ accumulation and Ca2+ depletion may occur in the extracellular spaces. 6) Modulation of EC coupling is governed by interactions between the myoplasmic Ca2(+)-binding proteins; specifically, the inotropic "positive staircase effect" may be explained by interactions between Ca2+ and Mg2+ at a competitive binding site on troponin. When considered in conjunction with the results of our model of primary pacemaking in the sinus venosus [Rasmusson et al., Am. J. Physiol. 259 (Heart Circ. Physiol. 28): H352-H369, 1990], this atrial model shows how the presence or absence of certain transmembrane currents can change action potential characteristics and consequently alter the relative influence of the various transporter-mediated and channel-mediated currents.