We used whole cell patch-clamp and microfluorimetric (indo 1) techniques to measure Ca 2+ current through L-type Ca 2+ channels (I(Ca)) and Ca 2+ 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 Ca 2+ concentration (r = 0.80, P <0.01). Slower-phase I(Ca) inactivation was not affected by ryanodine but was accelerated by increasing the availability of Ca 2+ to permeate the Ca 2+ channel. Thus Ca 2+ released from the sarcoplasmic reticulum (SR) was responsible for most I(Ca) inactivation during the first 50 ms of a depolarization to 0 mV, and thereafter inactivation by Ca 2+ permeating the channel predominated. Pure voltage- dependent inactivation had a much slower time course of development (τ > 2s) and played a smaller role than Ca 2+-dependent mechanisms over a duration comparable to that of an action potential. We conclude that human atrial myocytes show both voltage- and Ca 2+-dependent I(Ca) inactivation, that Ca 2+-dependent mechanisms predominate over the time course of an action potential, and that although both Ca 2+ released from the SR and Ca 2+ permeating Ca 2+ channels play a role, SR-released Ca 2+ is particularly important in early, rapid I(Ca) inactivation, whereas Ca 2+ permeating Ca 2+ channels is more important in the slower phase of Ca 2+-dependent inactivation.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||4 41-4|
|Publication status||Published - 1997|
- patch clamp
- permeating calcium ion
ASJC Scopus subject areas