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The effects of changing the time course of action potential repolarization on the amplitude and coupling interval of delayed afterdepolarizations were studied in small preparations of coronary sinus atrial fibers exposed to catecholamines. Repolarization was accelerated or retarded by current pulses passed through an intracellular microelectrode in the depolarizing or repolarizing direction. Acceleration of repolarization decreased the amplitude of delayed afterdepolarizations, prolonged their coupling interval to the action potential upstroke, and prevented triggered activity. Prolonging the time for repolarization increased afterdepolarization amplitude, shortened the coupling interval, and caused triggered activity. The afterdepolarization amplitude and coupling interval had a linear relationship to the duration of the action potential plateau. In some preparations, the action potential plateau increased spontaneously at stimulation rates that caused afterdepolarization amplitude to increase and triggering to occur, and this may have contributed to the occurrence of triggering. The effects of action potential repolarization on delayed afterdepolarizations suggest that pharmacological agents such as antiarrhythmic drugs which alter action potential duration should influence afterdepolarizations. Drugs which shorten action potential duration might prevent triggered activity from occurring, whereas drugs which prolong duration might cause triggering.

The time course of action potential repolarization affects delayed afterdepolarization amplitude in atrial fibers of the canine coronary sinus.