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Articles in PresS, published online ahead of print March 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00044.2002
Submitted on January 24, 2002
Accepted on March 4, 2002
1 Internal Medicine, University of California, Davis, Davis, CA, USA
2 Internal Medicine, Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: nchiamvimonvat{at}ucdavis.edu.
The properties of several components of outward K+ currents, their pharmacological and kinetics profiles as well as the respective molecular correlates have been identified in mouse cardiac myocytes. Surprisingly, little is known with regards 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 (TEA)-resistant transient outward current that is Ca2+-dependent. The current is carried by Cl- ions and is critically dependent on the Ca2+ influx via voltage-gated Ca2+ channel and the sarcoplasmic reticulum (SR) Ca2+ store. The current can be blocked by anion transport blockers; niflumic acid and 4,4' diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). 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-cell 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.
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