Inactivation of calcium channel current in calf cardiac Purkinje fibers is both voltage- and calcium-dependent, with calcium entry during depolarizing pulses increasing the rate of inactivation.
This preclinical study demonstrates that the inactivation of calcium channels in cardiac Purkinje fibers is mediated by both voltage-dependent and calcium-dependent mechanisms.
We have studied the influence of divalent cations on Ca channel current in the calf cardiac Purkinje fiber to determine whether this current inactivates by voltage- or Ca-mediated mechanisms, or by a combination of the two. We measured the reversal (or zero current) potential of the current when Ba, Sr, or Ca were the permeant divalent cations and determined that depletion of charge carrier does not account for time-dependent relaxation of Ca channel current in these preparations. Inactivation of Ca channel current persists when Ba or Sr replaces Ca as the permeant divalent cation, but the voltage dependence of the rate of inactivation is markedly changed. This effect cannot be explained by changes in external surface charge. Instead, we interpret the results as evidence that inactivation is both voltage and Ca dependent. Inactivation of Sr or Ba currents reflects a voltage-dependent process. When Ca is the divalent charge carrier, an additional effect is observed: the rate of inactivation is increased as Ca enters during depolarizing pulses, perhaps because of an additional Ca-dependent mechanism.
Kass et al. (1984) studied this question. Divalent cations (Ba, Sr, Ca) was evaluated on Inactivation of calcium channel current. Inactivation of calcium channel current in calf cardiac Purkinje fibers is both voltage- and calcium-dependent, with calcium entry during depolarizing pulses increasing the rate of inactivation.