The generation of the cardiac action potential: after the first millisecond

Abstract

After an initial, transient voltage- and time-dependent burst of sodium current (equivalent to that occurring in nerve), the membrane current of cardiac muscle reverses in sign to a maximum value that is orders of magnitude smaller than that seen in nerve. The membrane of cardiac muscle, rather than exchanging an increased permeability to sodium ions (Na+) for one to potassium ions (K+), appears to become relatively impermeable to a variety of ions. It is argued that in a tissue such as cardiac muscle where the time when the cell is active is comparable to that when it is quiescent, the current generated by the active electrogenic transport/exchange of Na+, K+, and Ca2+ must be comparable to the corresponding currents generated by the passive transport of these ions. Consequently, the complex voltage and time dependency of the membrane current on the time scale of repolarization and beyond is generated, at least in part, by the complex time and voltage dependency of these transport/exchange processes. Measurement of the electrochemical properties of such transport/exchange mechanisms must ultimately be made on the individual mechanisms in isolation, e.g., in artificial membrane systems, before their contribution to the generation of the cardiac action potential can be unequivocably determined.