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1 Division of Cardiovascular Medicine, Department of Medicine, University of California, Davis, California 95616; and 2 Division of Cardiology, University of Cincinnati, Cincinnati, Ohio 44267
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.
Ensemble-averaged 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.
cardiac
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