PKC activation reduces peak inward sodium current and prolongs current decay via a voltage-dependent action on the activation gate in sodium channel alpha-subunits.
PKC effects on cardiac Na channels remain preliminary in animal models; leaves open any role in human arrhythmogenesis or therapy.
The mechanism of modulation of sodium channel alpha-subunits (Type IIA) by a protein kinase C (PKC) activator was studied on single channel level. It was found that: (i) time constants for channel activation were prolonged; (ii) inactivation remained virtually unchanged; (iii) peak sodium inward current was reduced as evidenced by calculation of average sodium currents; and (iv) time constants for current activation and decay were prolonged. (i), (iii) and (iv) were voltage dependent, being most prominent at threshold potentials. The data show that a voltage dependent action on the activation gate can account for the observed reduction of peak inward sodium current and prolongation of current decay in macroscopic experiments.
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Schreibmayer et al. (1991) studied this question.
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