Key result
Aprindine decreases ventricular action potential Vmax via frequency-enhanced, use-dependent block.
Why the study?
The frequency- and voltage-dependent effects of aprindine on the upstroke velocity of action potential in cardiac muscle were not fully characterized.
Does aprindine reduce the upstroke velocity of action potentials in isolated guinea pig ventricular muscles?
Population
Isolated papillary muscles of guinea pig
Comparison
Aprindine at 10(-6)-10(-5) M vs no aprindine
Design
Preclinical experimental study
Authors
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Aprindine's frequency-dependent sodium channel effects in vitro support mechanistic studies; should not yet influence clinical antiarrhythmic use.
Does aprindine reduce the upstroke velocity of action potentials in isolated guinea pig ventricular muscles?
Aprindine demonstrates use-dependent and voltage-dependent inhibition of fast sodium channels in guinea pig ventricular muscle, providing a mechanistic basis for its antiarrhythmic effects.
Toyama et al. (1987) studied this question. Aprindine was evaluated on Vmax of the action potential. Aprindine caused a dose-dependent decrease in the Vmax of the action potential in guinea pig ventricular muscles, exhibiting use-dependent block that was enhanced at higher stimulation frequencies.
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