Abstract
The effect of dimethindene (DMI) on action potential and fast inward Na current (INa) of frog atrial fibres was studied using double sucrose gap voltage-clamp technique. DMI reduced the amplitude and maximum rate of rise of the action potentials without altering the resting membrane potential. The drug inhibited the fast Na conductance in a concentration-dependent manner, without changing the reversal potential. The shape of the current-voltage curve along the voltage axis remained unchanged in the presence of DMI. The time to peak of the INa was not significantly altered by the drug whereas the rate of the INa inactivation (tau h) was slowed. DMI shifted the steady-state inactivation curve of INa (h infinity) to more negative potentials, and increased the reactivation time constant of the sodium system (tau r). The inhibition of INa was use-dependent. The results suggest that DMI interacts with the inactivation mechanism of the sodium channel of the frog myocardium, and explain its favourable antiarrhythmic activity.
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