In human atrial myocytes, Ca2+-dependent mechanisms predominate over voltage-dependent mechanisms for L-type Ca2+ channel inactivation during the time course of an action potential.
We used whole cell patch-clamp and microfluorimetric (indo 1) techniques to measure Ca2+ current through L-type Ca2+ channels (I(Ca)) and Ca2+ transients in human atrial myocytes. During 1-s depolarizing pulses, I(Ca) inactivation was biexponential. The rate of rapid inactivation was slowed by ryanodine and was correlated with the rate of rise of cytoplasmic free Ca2+ concentration (r = 0.80, P 2 s) and played a smaller role than Ca2+-dependent mechanisms over a duration comparable to that of an action potential. We conclude that human atrial myocytes show both voltage- and Ca2+-dependent I(Ca) inactivation, that Ca2+-dependent mechanisms predominate over the time course of an action potential, and that although both Ca2+ released from the SR and Ca2+ permeating Ca2+ channels play a role, SR-released Ca2+ is particularly important in early, rapid I(Ca) inactivation, whereas Ca2+ permeating Ca2+ channels is more important in the slower phase of Ca2+-dependent inactivation.
Sun et al. (Tue,) reported a other. Ryanodine and Ca2+ availability manipulation was evaluated on Mechanisms of L-type Ca2+ channel inactivation. In human atrial myocytes, Ca2+-dependent mechanisms predominate over voltage-dependent mechanisms for L-type Ca2+ channel inactivation during the time course of an action potential.
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