Abstract

1. 1. Intracellular recording was used to examine the effects of 4-aminoquinoline (4-AQ) on action potentials of frog atrial myocardium depolarized by potassium. 2. 2. Elevating [K +] 0 to 12.5 mM resulted in decrease of resting membrane potential from 83 mV (normal Ringer) to 56 mV ( P <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 <0.02). 3. 3. 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. 4. 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 <0.001) increased amplitude, overshoot and duration of action potentials. 5. 5. These effects were attributed to an enhanced Ca 2+ 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.

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