DELAYED RECTIFIER K+ CURRENT IN RABBIT ATRIAL MYOCYTES

The role of delayed rectifier K+ current(s) (I-K) in rabbit left atrium was examined by applying the whole cell voltage-clamp technique to isolated single myocytes. Right-triangular waveforms, which mimic the shape of atrial action potentials (APs), and selective blockers were used to compare the contribution of I-K With Other K+ currents to repolarization of the APs. I-K measured at 34 degrees C in atrial myocytes was very small; the maximum peak amplitude of the tail current (I-K,I-tail) at -40 mV was similar to 50 pA. The I-K,I-tail was almost abolished in most cells (similar to 80%) by the application of 1 mu M E-4031, a class III antiarrhythmic drug. The E-4031-sensitive current recorded with the triangular command waveform showed strong inward rectification and had a maximum amplitude of similar to 30 pA at -40 mV. Total outward current elicited by triangular command pulses depended strongly on stimulation frequency. The main frequency-dependent component was a Ca2+-independent transient K+ current (I-t). I-t elicited by triangular pulses at 1 Hz was substantially reduced by 4-aminopyridine (4-AP) at potentials positive to 0 mV but was not changed significantly by 1 mu M E-4031; 100 mu M E-4031 reduced I-t by similar to 30%. The shape of the APs which were recorded from a single rabbit atrial cell strongly depended on the pulse frequency. Application of 1 mu M E-4031 increased action potential duration (APD) in >50% of cells examined but had little effect on the resting membrane potential (RMP). Application of 0.1 mM BaCl2 also lengthened APD and reduced RMP by similar to 20 mV. These results suggest that rabbit left atrial myocytes express an E-4O31-sensitive I-K which contributes to the late phase of AP repolarization at potentials between -10 and -70 mV. The 4-AP-sensitive I-t is the major outward current responsible for the early phase (positive to -10 mV) of AP repolarization even at 1-2 Hz.