Abstract
A class Ib antiarrhythmic drug, mexiletine (100 microM) significantly shortened the action potential duration (APD) of guinea-pig ventricular muscles and this effect was completely abolished in the presence of glibenclamide (50 microM), a blocker of the ATP-sensitive K+ channel (KATP). Mexiletine significantly increased the open probability of uridine diphosphate-primed KATP channels, recorded in inside-out patches of the ventricular cells. The results suggest that mexiletine shortens the APD of ventricular muscles, at least in part, via activation of KATP.
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Selected References
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