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Am J Physiol Heart Circ Physiol 278: H295-H299, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 1, H295-H299, January 2000

RAPID COMMUNICATION
Extracellular Ba2+ blocks the cardiac transient outward K+ current

Hong Shi1, Hui-Zhen Wang1, and Zhiguo Wang1,2

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 equal1 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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