Key result
Azimilide suppressed bi-directional Na+/Ca2+ exchange current in guinea-pig cardiac myocytes with an IC50 of 40-45 μM and significantly reduced ouabain-induced delayed afterdepolarizations.
Azimilide inhibits the Na+/Ca2+ exchanger at supratherapeutic concentrations and suppresses ouabain-induced delayed afterdepolarizations, providing insight into its antiarrhythmic mechanisms.
We examined the effect of azimilide, a class III antiarrhythmic drug, on Na(+)/Ca(2+) exchange current (I(NCX)) in guinea-pig cardiac single ventricular cells. External application of azimilide suppressed bi-directional I(NCX) in a concentration-dependent manner. IC(50) values for outward and inward I(NCX) were 45 and 40 µM, respectively, with Hill coefficients of 1. Azimilide attenuated I(NCX) in the presence of trypsin in the patch pipette, indicating that azimilide is a trypsin-insensitive NCX inhibitor. Delayed afterdepolarization induced by electrical stimulation with ouabain disappeared in the presence of 30 µM azimilide. We conclude that azimilide inhibits NCX at supratherapeutic concentrations.
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Watanabe et al. (2010) studied Arrhythmia (in vitro model). Azimilide vs. Control (absence of azimilide) was evaluated on Inhibition of Na+/Ca2+ exchange current (INCX) and ouabain-induced delayed afterdepolarizations (DADs) (p=<0.05). Azimilide suppressed bi-directional Na+/Ca2+ exchange current in guinea-pig cardiac myocytes with an IC50 of 40-45 μM and significantly reduced ouabain-induced delayed afterdepolarizations.
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