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1 Laboratory of Cardiac Cellular Research, Centre for Experimental Surgery and Anaesthesiology, and 2 Laboratory of Experimental Cardiology, University of Leuven, Leuven B-3000, Belgium
In cardiac cells that lack macroscopic
transient outward K+ currents (Ito),
the removal of extracellular Ca2+ can unmask
"Ito-like" currents. With the use of pig
ventricular myocytes and the whole cell patch-clamp technique, we
examined the possibility that cation efflux via L-type Ca2+
channels underlies these currents. Removal of extracellular
Ca2+ and extracellular Mg2+ induced
time-independent currents at all potentials and time-dependent currents
at potentials greater than 
50 mV. Either K+ or
Cs+ could carry the time-dependent currents, with reversal
potential of +8 mV with internal K+ and +34 mV with
Cs+. Activation and inactivation were voltage dependent
[Boltzmann distributions with potential of half-maximal value
(V1/2) = 24 mV and slope = 9
mV for activation; V1/2 = 58 mV and
slope = 13 mV for inactivation]. The time-dependent
currents were resistant to 4-aminopyridine and to DIDS but blocked by
nifedipine at high concentrations (IC50 = 2 µM) as
well as by verapamil and diltiazem. They could be increased by BAY
K-8644 or by isoproterenol. We conclude that the
Ito-like currents are due to monovalent cation flow through L-type Ca2+ channels, which in pig myocytes
show low sensitivity to nifedipine.
myocyte; channel; nonselective; pig
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