The rapid depolarization in cardiac muscle is due to
(B) Na++ # Resting membrane potential of individual mammalian cardiac muscle cells is about -90 mV (interior negative to exterior). Stimulation produces a propagated action potential that is responsible for initiating contraction. Depolarization proceeds rapidly, and an overshoot is present, as in skeletal muscle and nerve, but this is followed by a plateau before the membrane potential returns to the baseline. In mammalian hearts, depolarization lasts about 2 ms, but the plateau phase and repolarization last 200 ms or more. Repolarization is therefore not complete until the contraction is half over. With extracellular recording, the electrical events include a spike and a later wave that resemble the QRS complex and T wave of the ECG. As in other excitable tissues, changes in the external K+ concentration affect the resting membrane potential of cardiac muscle, whereas changes in the external Na+ concentration affect the magnitude of the action potential. Initial rapid depolarization and the overshoot (phase 0) are due to opening of voltage-gated Na+ channels similar to that occurring in nerve and skeletal muscle. Initial rapid repolarization (phase 1) is due to closure of Na+ channels. The subsequent prolonged plateau (phase 2) is due to a slower but prolonged opening of voltage-gated Ca2+ channels. Final repolarization (phase 3) to the resting membrane potential (phase 4) is due to closure of the Ca2+ channels and K+ efflux through various types of K+ channels. Voltage-gated Na+ channel in cardiac muscle has two gates--an outer gate that opens at the start of depolarization at a membrane potential of -70 to -80 mV; and an inner gate that then closes and precludes further influx until the action potential ends (Na+ channel inactivation). Slow Ca2+ channel is activated at a membrane potential of-30 to -40 mV. There are three types of K+ channels that proc jce repolarization. The first produces a transient, early outward current (lTO) that produces an early incomplete repolarizai on. Second is inwardly rectifying, ie, at plateau potentials it allows K+ influx but resists K+ efflux, and only at lower membrane potentials does it permit K+ efflux. Current it produces is called lKr. The third type is a slowly activating (delayed rectifying) type that produces a current called IKs. The sum of IKr and IKs is a small net outward current that increases with time and produces repolarization
Ca++
Na++
K++
Mg++
Misc.