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It has been previously demonstrated that melatonin exerts antiarrhythmic effects under conditions of ischemia and reperfusion in vivo by maintaining a relatively high conduction velocity in the myocardium. However, mechanistical details of this effect remain unclear, specifically whether melatonin affects myocardium directly or via systemic mediating signaling. The aim of the present study was to assess the impact of melatonin on the expression of genes encoding proteins potentially responsible for maintaining myocardial conduction in cultured cardiomyocytes. Ventricular cardiomyocytes isolated from neonatal rats were incubated with melatonin (100 µM) for 24 hours. Melatonin at a concentration of 100 µM enhanced the mRNA expression level of Scn5a gene and increased the amplitude of INa sodium current in cultured neonatal rat cardiomyocytes, but did not affect the parameters of steady-state activation and inactivation of INa. Thus, the present study demonstrated the direct effect of melatonin on sodium current in cardiomyocytes.
Durkina et al. (Mon,) studied this question.