Bailey J C, Elharrar V, Zipes D P
Annu Rev Med. 1978;29:417-26. doi: 10.1146/annurev.me.29.020178.002221.
The secondary inward current that flows through the slow channel is probably carried primarily by calcium ions. This current is responsible, in part, for the plateau phase of the cardiac action potential. Inward calcium current through the slow channel is essential to excitation-contraction coupling, and enhancement of this current exerts a positive inotropic effect. Transmembrane electrical potentials generated as a consequence of this slow inward current, so-called slow-channel depolarizations or slow responses, have been useful models in recent studies of cardiac autonomic interactions. The significance of the slow response in ventricular arrhythmias remains controversial and awaits more definitive experiments. The role of slow-channel depolarization as a basis for SA and AV nodal electrical activity is suggested by the electrophysiological similarities between these tissues and slow responses produced in vitro. This hypothesis is supported by the responses of these nodal tissues to interventions that augment of impede the slow inward current. More direct evidence in support of this notion may not be obtainable in the near future, since the critical voltage-clamp studies of ionic currents in SA and AV nodes are not technically feasible at this time.
流经慢通道的继发性内向电流可能主要由钙离子携带。该电流部分地负责心脏动作电位的平台期。通过慢通道的内向钙电流对于兴奋 - 收缩偶联至关重要，并且该电流的增强会产生正性肌力作用。由这种缓慢内向电流产生的跨膜电位，即所谓的慢通道去极化或慢反应，在最近关于心脏自主神经相互作用的研究中是有用的模型。慢反应在室性心律失常中的意义仍存在争议，有待更明确的实验。这些组织与体外产生的慢反应之间的电生理相似性提示了慢通道去极化作为窦房结和房室结电活动基础的作用。这些结性组织对增加或阻碍缓慢内向电流的干预的反应支持了这一假设。由于目前对窦房结和房室结离子电流进行关键的电压钳研究在技术上不可行，因此在不久的将来可能无法获得支持这一观点的更直接证据。
