Computational modeling of sinoatrial node cells reveals that pacemaker rhythm is highly sensitive to L-type Ca2+ and rapid delayed rectifying K+ channel conductances, highlighting their potential as targets for antiarrhythmic therapies.
Pacemaker sensitivity to ICa,L and IKr identifies candidate targets; leaves open translation from animal modeling to clinical use.
As a cardiac pacemaker, sinoatrial node spontaneously generates periodic electrical signals (action potentials) in its cells. The action potential generation is deeply related to various ion channels in cell membranes, and the abnormalities of ion channels cause sinus arrhythmia. We use the Zhang model of sinoatrial node cells to investigate the relation between pacemaker rhythm (frequency of action potential generation) and ion channels. The Zhang model is described by the Hodgkin-Huxley-type nonlinear ordinary differential equations, and its parameter values vary between periphery and center cells of sinoatrial node. We analyze the bifurcation structure of the Zhang model, and investigate the variability of pacemaker rhythm and its sensitivity on ion channel conductance changes for both periphery and center cells. Moreover, these results are compared with the previous results of another sinoatrial node cell model: Yanagihara-Noma-Irisawa model.
No takes yet. Share an insight, caveat, or question.
Pan et al. (2011) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: