The properties of several components of outward K+ currents, including the pharmacological and kinetics profiles as well as the respective molecular correlates, have been identified in mouse cardiac myocytes. Surprisingly little is known with regard to the Ca2+-activated ionic currents. We studied the Ca2+-activated transient outward currents in mouse ventricular myocytes. We have identified a 4-aminopyridine (4-AP)- and tetraethyl ammonium-resistant transient outward current that is Ca2+ dependent. The current is carried by Cl- and is critically dependent on Ca2+ influx via voltage-gated Ca2+ channels and the sarcoplasmic reticulum Ca2+ store. The current can be blocked by the anion transport blockers niflumic acid and 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid. Single channel recordings reveal small conductance channels (∼1 pS in 140 mM Cl-) that can be blocked by anion transport blockers. Ensembleaveraged current faithfully mirrors the transient kinetics observed at the whole level. Niflumic acid (in the presence of 4-AP) leads to prolongation of the early repolarization. Thus this current may contribute to early repolarization of action potentials in mouse ventricular myocytes.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||1 52-1|
|State||Published - 2002|
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