Inactivation of sodium channels in isolated myocardial mouse cells.

Inactivation of sodium currents is investigated in single myocardial mouse cells by the use of a one suction pipette voltage clamp technique. Semilogarithmic plots of the decay phase of sodium currents show two phases and analysis yields a fast (tau h1) and a slow (tau h2) time constant. At increased depolarization the contribution of tau h2 is decreased. Increasing the temperature from 22.0 +/- 0.5 degrees C to 36.5 +/- 0.5 degrees C influences tau h1 and tau h2 to the same extent. The Q10 values were 2.28 +/- 0.32 for tau h1 and 2.46 +/- 0.35 (mean +/- SD) for tau h2. Between -50 and -20 mV the time course of current decay is substantially faster than inactivation induced by prepulses. Onset of inactivation by the prepulse protocol needs two time constants (tau c1, tau c2) for a satisfactory description. Both decrease steeply with increasing depolarization. For small depolarizations, tau c2 values are in the range of several seconds. Recovery from inactivation by short prepulses (40 ms) could be described by two exponentials (tau r1, tau r2). For longer prepulses (1,000 ms) a very slow component, tau r3, was observed indicating a history dependence of inactivation. Delay time constants for the onset of inactivation (tau dc) are determined between -50 and -20 mV. The more depolarizing voltages generate smaller delay times (0.55 +/- 0.10 ms at -20 mV, mean +/- SD) but larger deviations from the exponential time course. Delay in recovery from inactivation (time constant tau dr) has the value 2.0 +/- 0.7 ms (mean +/- SD) at -80 mV and decreases at more hyperpolarizing potentials. The remaining series resistance at maximum compensation was calculated as 80 k omega. Its influence on the sensitive delay in the double pulse inactivation is discussed.