An investigation of the role played by the E-4031-sensitive (rapid delayed rectifier) potassium current in isolated rabbit atrioventricular nodal and ventricular myocytes.

Abstract

The aim of this study was to measure and compare the profile of rapid delayed rectifier potassium current (IKr) elicited by action potential (AP) waveforms applied to isolated rabbit atrioventricular nodal (AVN) and ventricular myocytes. All measurements were made using whole-cell patch-clamp recordings at 37 degrees C. In AVN myocytes, IKr 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 activation relation of 6.5 +/- 0.77 mV (n = 7). During AVN APs, IKr 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 IKr remained which decayed during the pacemaker depolarisation, consistent with a role for the current in generating AVN pacemaker activity. In ventricular myocytes IKr was small at the beginning of the AP, and increased slowly during the AP plateau. Measurement of Ba-sensitive-inward rectifier K current (IK1) in ventricular myocytes revealed that IK1 rapidly increased during the final AP repolarisation phase, whilst IKr declined. It is concluded that IKr may participate in both AP repolarisation and the pacemaker depolarisation in AVN cells, whilst in ventricular myocytes, IKr and IK1 participate in controlling early and final AP repolarisation respectively.