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1 Research Center, Montreal Heart Institute, Montreal, Quebec H1T 1C8; and 2 Department of Medicine, University of Montreal, Montreal, Quebec, Canada H3C 3J7
Ba2+ is widely used as a tool in patch-clamp
studies because of its ability to block a variety of K+
channels and to pass Ca2+ channels. Its potential ability
to block the cardiac transient outward K+ current
(Ito) has not been clearly documented. We performed
whole cell patch-clamp studies in canine ventricular and atrial
myocytes. Extracellular application of Ba2+ produced potent
inhibition of Ito with an IC50 of ~40
µM. The effects were voltage independent, and the inactivation
kinetics were not altered by Ba2+. The potency of
Ba2+ was ~10 times higher than that of 4-aminopyridine (a
selective Ito blocker with an IC50 of
430 µM) under identical conditions. By comparison, Ba2+
blockade of the inward rectifier K+ current was voltage
dependent; the IC50 was ~20 times lower (2.5 µM) than
that for Ito when determined at
100 mV and was comparable to Ito as
determined at 60 mV (IC50 = 26 µM).
Ba2+ concentrations of 
1 mM or higher failed to block
ultrarapid delayed rectifier K+ current. Our data suggest
that Ba2+ can be considered a potent blocker of
Ito.
patch clamp; cardiac myocytes; 4-aminopyridine; inward rectifier potassium current; ultrarapid delayed rectifier potassium current
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