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Objectives The effects of carvedilol on sodium current (INa) were investigated in isolated adult rat ventricular myocytes. Methods Single ventricular myocytes were enzymatically dissociated. INawas recorded by whole-cell patch-clamp recording technique. Results 1. Carvedilol reversibly inhibited INa in a concentration-dependent manner, with an IC50of (6.35± 0.40) mol·L-1. 2. This inhibition was voltage- and frequency-dependent. 3. Carvedilol decreased the peak of the I-V relationship curve at -35 mV from (17.31± 1.68) pA/pF to (6.58± 1.35) pA/pF, but did not change active potential, peak potential and the reverse potential significantly. 4. The steady-state inactivation curve of INa was shifted to more negative potentials. Conclusions Carvedilol inhibits INa in adult rat ventricular myocytes by mechanisms involving preferential interaction with the inactivated state of sodium channel.
Objectives The effects of carvedilol on sodium current (INa) were investigated in isolated adult rat ventricular myocytes. Methods Single ventricular myocytes were enzymatically dissociated. INawas recorded by whole-cell patch-clamp recording technique. Results 1. Carvedilol reversibly inhibited INa in a concentration -dependent manner with an IC50of (6.35 ± 0.40) mol·L-1. 2. This inhibition was voltage- and frequency-dependent. 3. Carvedilol decreased the peak of the IV relationship curve at -35 mV from (17.31 ± 1.68 ) pA / pF to (6.58 ± 1.35) pA / pF, but did not change the active potential, peak potential and the reverse potential significantly. 4. The steady-state inactivation curve of INa was shifted to more negative potentials. Conclusions Carvedilol inhibits INa in adult rat ventricular myocytes by mechanisms involving preferential interaction with the inactivated state of sodium channel.