Publication details

Changes of action potential configuration under ethanol related to its effects on inward rectifier currents in rat and guinea-pig cardiomyocytes



Year of publication 2015
Type Conference abstract
MU Faculty or unit

Faculty of Medicine

Description Purpose: Alcohol consumption is known to cause electrocardiographic changes, arrhythmias, and even the sudden cardiac death. Knowledge about ethanol effects on cardiac inward rectifier currents, which play an important role in arrhythmogenesis, is rather small and impact of their ethanol-induced changes on the action potential (AP) configuration has not been studied yet. Hence, we aimed to analyse changes of AP configuration in the presence of ethanol and correlate them to ethanol-induced changes of inward rectifier currents, namely IK1 and acetylcholine-sensitive potassium current IK(Ach). Methods: Experiments were performed on enzymatically isolated rat and guinea-pig cardiomyocytes at room temperature in the presence of 2 mM Co2+ to inhibit the calcium current ICa (to avoid a contribution of its changes). Results: In the presence of 20 mM (~0.9‰) ethanol, all AP parameters remained stable in both rat and guinea-pig atrial myocytes except for AP duration (APD) which was slightly but significantly shortened. Since ethanol-induced IK1 changes were subtle in rat atrial cells, the observed APD shortening was likely caused by a significant increase of the constitutively-active component of IK(Ach) (rat: from -0.66 ± 0.12 pA/pF in control to -1.19 ± 0.20 pA/pF at 20 mM ethanol, n = 10; guinea-pig: from -0.46 ± 0.11 pA/pF in control to -0.78 ± 0.20 pA/pF at 20 mM ethanol, n = 4). In contrast to the atrial myocytes, a dual effect on APD was apparent in rat ventricular myocytes – a slight APD prolongation at very low concentrations (0.8 mM, ~0.04 ‰) and APD shortening at concentrations above 8 mM (~0.4‰). According to mathematical simulations, these changes under low ethanol concentrations are predominatly caused by ethanol-induced changes of IK1, namely an inhibition at 0.8 mM ethanol and an increase at ethanol concentrations above 8 mM. We conclude that APD changes induced by ethanol at clinically-relevant concentrations seem to be comparable in rat and guinea-pig atrial myocytes and, in the absence of ICa, are mainly caused by the ethanol effect on cardiac inward rectifier currents, namely on IK(Ach) and IK1 in atrial and ventricular cardiomyocytes, respectively.
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