The electrophysiologic effects of aprindine HCl (N-[3-(diethylamino) propyl]-N-phenyl-2-indanamine) were studied on normal Purkinje fibers, on Purkinje fibers superfused with Tyrode's solution containing 22 mM KCl and isoproterenol (1 x 10-5M) and on Purkinje fibers in which transient depolarizations were induced by exposure to acetylstrophanthidin (1.7- 2 x 10-7M). Results: 1) In normal Purkinje fibers, aprindine (3 x 10-6M) significantly reduced the action potential amplitude and dV/dtmax, shortened the action potential duration but did not alter the resting membrane potential or the plateau amplitude. 2) Slow responses induced in K-depolarized, isoproterenol-treated fibers were unchanged by aprindine (3 x 10-6 - 1 x 10-5M). 3) Transient depolarizations were suppressed by aprindine at a dose of 2 x 10-6M. 4) Isoproterenol failed to restore transient depolarizations after suppression with aprindine. Conclusions: These experiments suggest that aprindine does not have slow channel blocking properties and that an inward current through the slow channel cannot be considered as the sole basis for the digitalis-induced transient depolarizations. (Supported in part by American Heart Association, Indiana Affiliate, Inc.).
|Original language||English (US)|
|Pages (from-to)||No. 783|
|State||Published - Jan 1 1977|
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