Characterization of the sodium currents in isolated human cardiocytes.

The whole-cell recording technique was used to register Na+ currents from 403 atrial cardiocytes isolated from 80 human biopsies. With intracellular [Na+] ([Na+]i) raised to 70 mM, and at physiological extracellular [Na+] ([Na+]e, 145 mM) and room temperature, the Na+ currents were small enough for the error of the voltage clamp not to exceed 2 mV (series resistances 0.4-2 M omega). The threshold potential of the Na+ current was -64.0 +/- 7.7 mV. The peak amplitude was at -30.0 +/- 6.2 mV. The time course of fast inactivation was satisfactorily described with a single exponential. The time constant of inactivation was 2.0 ms at -55 mV and asymptotically approached 0.2 ms at positive membrane potentials. The steady-state inactivation curve was well fitted by a single Boltzmann distribution. Increasing the prepulse duration from 32 to 512 ms shifted the inflexion point of the curve from -61.7 +/- 6.4 to -72.2 +/- 2.6 mV. The time course of slow inactivation was also well described by a single exponential, the time constant ranging from 76.1 +/- 29.3 ms at -115 mV to 18.6 +/- 7.8 ms at -55 mV. Fitting the time course of recovery from inactivation required two time constants. At a recovery potential of -135 mV these were 1.6 +/- 0.2 and 8.6 +/- 2.9 ms and 15.9 +/- 9.4 and 53.2 +/- 33.3 ms at -95 mV. A 50% block of the Na+ currents was achieved by tetrodotoxin at 10 microM. It is concluded that the properties of human cardiac Na+ channels are similar to those of the juvenile Na+ channels of human skeletal muscle.