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 (IK) 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 IK in morphologically normal cells from the atrioventricular node (AVN) and ventricle of the rabbit heart. Cells were held at -40 mV and 5 microM external nifedipine was used to block L-type calcium current (ICa,L). Significant IK 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 IK 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 IK 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 IK and this suggested that only the rapid component of IK, called IKr, was present in either cell type. Moreover, IK tails after pulses to all potentials were blocked completely by E-4031, a selective blocker of IKr. The reversal potential of IK 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 IK channel were highly selective for K. The time constants for deactivation of IK 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 IK in AVN cells was a distinguishing feature and suggests that there may be differences in the IKr channel protein between ventricular and AVN cells.
Howarth
F C
FC
Department of Physiology, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK.
Levi
A J
AJ
Hancox
J C
JC
D000200:Action Potentials; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001283:Atrioventricular Node / Q000737:chemistry / Q000166:cytology; D006352:Heart Ventricles / Q000737:chemistry / Q000166:cytology; D008564:Membrane Potentials / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D018408:Patch-Clamp Techniques; D010880:Piperidines / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011674:Pulse / Q000502:physiology; D011725:Pyridines / Q000494:pharmacology; D011817:Rabbits
D000889:Anti-Arrhythmia Agents; D010880:Piperidines; D015221:Potassium Channels; D011725:Pyridines; C063968:E 4031