Acute and chronic effects of taurine magnesium coordination compound on cardiac sodium channel Nav1.5

Abstract It has been previously demonstrated that taurine magnesium coordination compound (TMCC) produces antiarrhythmic effects in vivo. The present study investigated the acute and chronic effect of TMCC on sodium channels in HEK cells stably expressing human cardiac Nav1.5 sodium channels. The current amplitude, activation and inactivation kinetics, recovery time from inactivation, and use‑dependent block of sodium channels were analyzed using the whole‑cell patch clamp technique. Western blotting was used to analyze Nav1.5 expression following chronic TMCC treatment. In HEK cells expressing Nav1.5 channels, TMCC acutely inhibited Na+ currents in a dose‑dependent manner. In addition, acute application of TMCC shifted the activation and inactivation curves, and prolonged the recovery time from inactivation, but did not exhibit a use‑dependent block of Nav1.5. By contrast, chronic TMCC treatment only produced a use‑dependent block of Nav1.5 and downregulated Nav1.5 expression. The results of the present study suggested that TMCC may produce antiarrhythmic actions via acute inhibition of sodium channel currents and chronic downregulation of Nav1.5 expression.