An investigation of the role played by the E-4031-sensitive (rapid delayedrectifier) potassium current in isolated rabbit atrioventricular nodal andventricular myocytes

The aim of this study was to measure and compare the profile of rapid delay ed rectifier potassium current (I-Kr) elicited by action potential (AP) wav eforms applied to isolated rabbit atrioventricular nodal (AVN) and ventricu lar myocytes. All measurements were made using whole-cell patch-clamp recor dings at 37 degrees C. In AVN myocytes, I-Kr during voltage steps and slow ramp depolarisations showed "inward rectification" (characteristic for this channel) at positive potentials. The E-4031-sensitive current showed half- maximal activation at -10.8+/-0.86 mV, with a slope factor for the activati on relation of 6.5+/-0.77 mV (n=7). During AVN APs, I-Kr rapidly reached a peak after the AP upstroke and remained at similar amplitude until late in AP repolarisation. At the maximum diastolic potential following the AVN AP, a component of I-Kr remained which decayed during the pacemaker depolarisa tion, consistent with a role for the current in generating AVN pacemaker ac tivity. In ventricular myocytes I-Kr was small at the beginning of the AP, and increased slowly during the AP plateau. Measurement of Ba-sensitive-inw ard rectifier K current (I-K1) in ventricular myocytes revealed that I-K1 r apidly increased during the final AP repolarisation phase, whilst I-Kr decl ined. It is concluded that I-Kr may participate in both AP repolarisation a nd the pacemaker depolarisation in AVN cells, whilst in ventricular myocyte s, I-Kr and I-K1 participate in controlling early and final AP repolarisati on respectively.