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* Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada; and Department of Bioengineering, Whitaker Institute of Biomedical Engineering, University of California, San Diego, La Jolla, California
Correspondence: Address reprint requests to Dr. Wayne R. Giles, Dept. of Bioengineering, Whitaker Institute of Biomedical Engineering, University of California, San Diego, La Jolla, CA 92093-0412. Tel.: 858-822-4424; Fax: 858-534-4535; E-mail: wgiles{at}bioeng.ucsd.edu.
K+ currents expressed in freshly dispersed rat ventricular fibroblasts have been studied using whole-cell patch-clamp recordings. Depolarizing voltage steps from a holding potential of –90 mV activated time- and voltage-dependent outward currents at membrane potentials positive to 
–30 mV. The relatively slow activation kinetics exhibited strong dependence on the membrane potential. Selected changes in extracellular K+ concentration ([K+]o) revealed that the reversal potentials of the tail currents changed as expected for a K+ equilibrium potential. The activation and inactivation kinetics of this K+ current, as well as its recovery from inactivation, were well-fitted by single exponential functions. The steady-state inactivation was well described by a Boltzmann function with a half-maximal inactivation potential (V0.5) of –24 mV. Increasing [K+]o (from 5 to 100 mM) shifted this V0.5 in the hyperpolarizing direction by –11 mV. Inactivation was slowed by increasing [K+]o to 100 mM, and the rate of recovery from inactivation was decreased after increasing [K+]o. Block of this K+ current by extracellular tetraethylammonium also slowed inactivation. These [K+]o-induced changes and tetraethylammonium effects suggest an important role for a C-type inactivation mechanism. This K+ current was sensitive to dendrotoxin-I (100 nM) and rTityustoxin K
(50 nM).
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