Computer simulation demonstrated that suppression of the rapid potassium current leads to the recovery of normal oscillation mode of ion dynamics in a pacemaker cell.
A computer simulation of rabbit sinoatrial node cells demonstrates that suppressing the rapid potassium current restores normal oscillation, providing a mechanistic model for class III antiarrhythmic agents.
Abstract—This paper reports an analysis of a stochastic model of ion dynamics in the cardiac pacemaker cell within the framework of the generalized two-oscillator Maltsev–Lakatta model, including the electron-conformational model of ryanodine receptors. It has been demonstrated that generation of an action potential depends significantly on the nature of the interaction between the external membrane and the internal (Ca2+ clock) oscillators. Constructive interaction between oscillators leads to the formation of a stable action potential, while destructive interaction leads to parasitic effects, in particular, to arrhythmias. The effects of the model parameters that are characteristic of the rabbit sinoatrial heart node on the shape of the time dependence of the cell membrane potential has been investigated. The conditions under which spontaneous transition to the abnormally fast oscillatory mode takes place have been determined and the mechanism of this transition has been described; the pacemaker cell behavior in tachycardia has actually been simulated. It has been demonstrated that suppression of the rapid potassium current leads to the recovery of the normal oscillation mode of ion dynamics in a pacemaker cell, which corresponds to the mode of action of class III antiarrhythmic agents.
Zorin et al. (Mon,) conducted a other in Cardiac Arrhythmias. Suppression of the rapid potassium current was evaluated on Recovery of the normal oscillation mode of ion dynamics. Computer simulation demonstrated that suppression of the rapid potassium current leads to the recovery of normal oscillation mode of ion dynamics in a pacemaker cell.