The effect of 4-aminoquinoline on frog atrial myocardium depolarized by potassium

Intracellular recording was used to examine the effects of 4-aminoquinoline (4-AQ) on action potentials of frog atrial myocardium depolarized by potassium. Elevating [K+]0 to 12.5 mM resulted in decrease of resting membrane potential from 83 mV (normal Ringer) to 56 mV (P less than 0.001). Under these conditions, verapamil diminished amplitude, overshoot and duration of action potentials, whereas 4-AQ depressed overshoot and prolonged action potential duration (P less than 0.02). Action potentials recorded in 20 mM K+ (isoproterenol added) exhibited a mean resting potential of 38 mV and also a reduced amplitude and duration. Verapamil caused a rapid blockade of the electrophysiological response, suggesting that action potentials were mediated by a current carried by calcium ions. 4-AQ applied in two concentrations (0.25 and 0.5 mM) on atrial trabeculae exposed to 20 mM K+-isoproterenol partially restored resting membrane potential and significantly (P less than 0.001) increased amplitude, overshoot and duration of action potentials. These effects were attributed to an enhanced Ca2+ entrance induced either by a direct action upon voltage-sensitive calcium channels, or resulting from a prolonged action potential due to blockade of potassium conductance.