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Melatonin Upregulates Sodium Channel Nav1.5 in Cultured Neonatal Rat Cardiomyocytes
A Durkina1, M Gonotkov, A Furman
1Department of Biomedical Technology, Faculty of Biomedical Engineering, Czech Technical University in Prague, Kladno, Czech Republic.
Physiological Research
|December 17, 2025
Summary
Melatonin directly impacts heart cells by boosting the Scn5a gene and increasing sodium current amplitude in cultured cardiomyocytes. This finding clarifies melatonin's antiarrhythmic mechanisms.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Pharmacology
Background:
- Melatonin demonstrates in vivo antiarrhythmic effects during ischemia-reperfusion by preserving myocardial conduction velocity.
- The precise mechanisms, particularly direct versus systemic effects on the myocardium, remain incompletely understood.
Purpose of the Study:
- To investigate the direct impact of melatonin on gene expression related to myocardial conduction in cultured cardiomyocytes.
- To elucidate the role of melatonin in regulating ion channel function within cardiac cells.
Main Methods:
- Neonatal rat ventricular cardiomyocytes were cultured and treated with 100 µM melatonin for 24 hours.
- Quantitative real-time PCR was used to assess Scn5a mRNA expression levels.
- Electrophysiological recordings (patch-clamp) were performed to measure the INa sodium current amplitude and its gating properties.
Main Results:
- Melatonin treatment significantly enhanced the mRNA expression of the Scn5a gene in cultured cardiomyocytes.
- A notable increase in the amplitude of the INa sodium current was observed following melatonin exposure.
- Melatonin did not alter the steady-state activation or inactivation parameters of the INa current.
Conclusions:
- This study provides direct evidence that melatonin acts on cardiomyocytes to modulate sodium channel function.
- Melatonin's enhancement of Scn5a expression and INa amplitude contributes to its antiarrhythmic properties by directly influencing myocardial electrical activity.
