Extracellular Ba(2+) blocks the cardiac transient outward K(+) current.
Ba(2+) is widely used as a tool in patch-clamp studies because of its ability to block a variety of K(+) channels and to pass Ca(2+) channels. Its potential ability to block the cardiac transient outward K(+) current (I(to)) has not been clearly documented. We performed whole cell patch-clamp studies in canine ventricular and atrial myocytes. Extracellular application of Ba(2+) produced potent inhibition of I(to) with an IC(50) of approximately 40 microM. The effects were voltage independent, and the inactivation kinetics were not altered by Ba(2+). The potency of Ba(2+) was approximately 10 times higher than that of 4-aminopyridine (a selective I(to) blocker with an IC(50) of 430 microM) under identical conditions. By comparison, Ba(2+) blockade of the inward rectifier K(+) current was voltage dependent; the IC(50) was approximately 20 times lower (2.5 microM) than that for I(to) when determined at -100 mV and was comparable to I(to) as determined at -60 mV (IC(50) = 26 microM). Ba(2+) concentrations of </=1 mM or higher failed to block ultrarapid delayed rectifier K(+) current. Our data suggest that Ba(2+) can be considered a potent blocker of I(to).
Shi
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Research Center, Montreal Heart Institute, Montreal, Quebec H1T 1C8.
Wang
H Z
HZ
Wang
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D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D016275:Atrial Function; D001464:Barium / Q000494:pharmacology / Q000502:physiology*; D002469:Cell Separation; D004285:Dogs; D004553:Electric Conductivity; D005110:Extracellular Space / Q000378:metabolism*; D006321:Heart / Q000502:physiology*; D009206:Myocardium / Q000166:cytology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000037:antagonists & inhibitors* / Q000502:physiology*; D016276:Ventricular Function
D001464:Barium; D015761:4-Aminopyridine; D011188:Potassium