Why the study?
Do diltiazem and nifedipine inhibit repolarization K+ currents in human atrial myocytes?
Do diltiazem and nifedipine inhibit repolarization K+ currents in human atrial myocytes?
Diltiazem and nifedipine inhibit transient outward and ultra-rapid delayed rectifier potassium currents in human atrial myocytes, suggesting an open channel block mechanism.
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May modulate atrial repolarization beyond calcium blockade; hypothesis-generating in animal models and requires human validation before clinical consideration.
It is unknown whether the widely used L-type Ca(2+) channel antagonists diltiazem and nifedipine would block the repolarization K(+) currents, transient outward current (I(to1)) and ultra-rapid delayed rectifier K(+) current (I(Kur)), in human atrium. The present study was to determine the effects of diltiazem and nifedipine on I(to1) and I(Kur) in human atrial myocytes with whole-cell patch-clamp technique. 2. It was found that diltiazem substantially inhibited I(to1) in a concentration-dependent manner, with an IC(50) of 29.2+/-2.4 microM, and nifedipine showed a similar effect (IC(50)=26.8+/-2.1 muM). The two drugs had no effect on voltage-dependent kinetics of the current; however, they accelerated I(to1) inactivation significantly, suggesting an open channel block. 3. In addition, diltiazem and nifedipine suppressed I(Kur) in a concentration-dependent manner (at +50 mV, IC(50)=11.2+/-0.9 and 8.2+/-0.8 microM, respectively). These results indicate that the Ca(2+) channel blockers diltiazem and nifedipine substantially inhibit I(to1) and I(Kur) in human atrial myocytes.
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Gao et al. (2005) studied this question.
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