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 μM external nifedipine was used to block L-type calcium current (I(Ca,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 I(K) 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.