Yanagihara K, Noma A, Irisawa H
Jpn J Physiol. 1980;30(6):841-57. doi: 10.2170/jjphysiol.30.841.
The pacemaker activity of the S-A node cell was explained by reconstructing the pacemaker potential using a Hodgkin-Huxley type mathematical model which was based on the reported voltage clamp data. In this model four dynamic currents, the sodium current iNa, the slow inward current, is, the potassium current, iK, and the hyperpolarization-activated current, ih, in addition to a time-dependent leak current, i1 were included. The model simulated the spontaneous action potential the current voltage relationship, and the voltage clamp experiment in normal Tyrode solution of the rabbit S-A node. Furthermore, the changes of activity induced by the potassium current blocker Ba2+, by applying constant current, acetylcholine, and epinephrine were also reconstructed. It was strongly suggested that the pacemaker depolarization in the S-A node cell is mainly due to a gradual increase of iS during diastole, and that the contribution of iK is much less compared to the potassium current iK2 in the Purkinje fiber pacemaker depolarization. The rising phase of the action potential was due to iS and the plateau phase is determined by both the inactivation of iS and activation of iK.
通过使用基于所报道的电压钳数据的霍奇金-赫胥黎类型数学模型重建起搏电位，解释了窦房结细胞的起搏活动。在该模型中，除了一个随时间变化的漏电流i1外，还包括四种动态电流，即钠电流iNa、缓慢内向电流is、钾电流iK和超极化激活电流ih。该模型模拟了兔窦房结在正常台氏液中的自发动作电位、电流-电压关系以及电压钳实验。此外，还重建了钾电流阻滞剂Ba2+、施加恒定电流、乙酰胆碱和肾上腺素引起的活动变化。强烈提示，窦房结细胞的起搏去极化主要是由于舒张期is逐渐增加，并且与浦肯野纤维起搏去极化中的钾电流iK2相比，iK的贡献要小得多。动作电位的上升期归因于is，而平台期由is的失活和iK的激活共同决定。
