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Mexiletine‐induced shortening of the action potential duration of ventricular muscles by activation of ATP‐sensitive K + channels
Author(s) -
Sato Toshiaki,
Shigematsu Sakuji,
Arita Makoto
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb16342.x
Subject(s) - mexiletine , glibenclamide , chemistry , medicine , electrophysiology , mechanism of action , pharmacology , biophysics , endocrinology , biology , biochemistry , in vitro , diabetes mellitus
A class Ib antiarrhythmic drug, mexiletine (100 μ M ) significantly shortened the action potential duration (APD) of guinea‐pig ventricular muscles and this effect was completely abolished in the presence of glibenclamide (50 μ M ), a blocker of the ATP‐sensitive K + channel (K ATP ) ‐ Mexiletine significantly increased the open probability of uridine diphosphate‐primed K ATP 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 K ATP .