Abstract
Dysregulation of intracellular Ca2+ homeostasis is associated with various pathological conditions and arrhythmogenesis of the heart. The objective of this study was to investigate the effects of an acute increase in intracellular Ca2+ concentration ([Ca2+]i) on the electrophysiology of ventricular myocytes by mimicking intracellular Ca2+ overload. The [Ca2+]i was clamped to either a controlled (65–100 nmol L−1) or increased (1 μmol L−1) level. The transmembrane action potentials and ionic currents were recorded using whole-cell patch clamp techniques. We found that the acute increase in [Ca2+]i shortened the action potential duration, reduced the action potential amplitude, maximum depolarization velocity and resting membrane potential, caused delayed after-depolarizations (DADs), and triggered activity—compared with these parameters in the control. The increased [Ca2+]i augmented late INa in a time-dependent manner, reduced ICaL and IK1, and increased IKr but not IKs. The results of this study can be used to explain calcium overload-induced ventricular arrhythmias.
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Fan, X., Ma, J., Wan, W. et al. Increased intracellular calcium concentration causes electrical turbulence in guinea pig ventricular myocytes. Sci. China Life Sci. 54, 240–247 (2011). https://doi.org/10.1007/s11427-011-4146-1
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DOI: https://doi.org/10.1007/s11427-011-4146-1