Characteristics of the delayed rectifier K current compared in myocytes isolated from the atrioventricular node and ventricle of the rabbit heart

The delayed rectifier potassium current (I-K) is known-to be important in action potential repolarisation and may contribute to the diastolic pacemaker depolarisation in pacemaker cells from the heart. In this study, using whole-cell patch clamp, we investigated the characteristics of I-K in morphologically normal cells from the atrioventricular node (AVN) and ventricle of the rabbit heart. Cells were held at -40 mV and 5 mu M external nifedipine was used to block L-type calcium current (I-Ca,I-L) Significant I-K was observed with pulses to potentials more positive than -30 mV. The steady-state activation curve in both cell types showed maximal activation at between +10 and +20 mV. Half-maximal activation of I-K occurred at -4.9 and -4.1 mV with slope factors of 8.3 and 12.4 mV in ventricular and AVN cells, respectively. Using pulses of increasing duration, significant I-K tails after repolarisation from +40 mV were observed with pulses of 20 ms and increased with pulses up to 100-120 ms in both cell types. Pulses of longer duration did not activate further L and this suggested that only the rapid component of I-K, called I-Kr, was present in either cell type. Moreover, I-K tails after pulses to all potentials were blocked completely by E-4031, a selective blocker of I-Kr. The reversal potential of I-K varied with the concentration of external K. Superfusion of AVN cells with medium containing 4, 15 and 40 mM [K+](o) resulted in reversal potentials of -81, -56 and -32 mV, respectively, which are close to values predicted if the I-K channel were highly selective for K. The time constants for deactivation of I-K in ventricle and AVN on return to -40 mV after a 500-ms activating pulse to + 60 mV were 480 ms and 230 ms, respectively. The faster deactivation of I-K in AVN cells was a distinguishing feature and suggests that there may be differences in the I-Kr, channel protein between ventricular and AVN cells.