© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Pacing-induced heart failure causes a reduction of delayed rectifier potassium currents along with decreases in calcium and transient outward currents in rabbit ventricle
aDepartment of Circulation, Division of Regulation of Organ Function, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan
bDepartment of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands
* Corresponding author. Tel.: +81-52-789-3871; fax: +81-52-789-3890 ikodama{at}riem.nagoya-u.ac.jp
Objective: Heart failure in patients and in animal models is associated with action potential prolongation of the ventricular myocytes. Changes in several membrane currents have been already demonstrated to underlie this prolongation. However, information on the two components (IKr and IKs) of the delayed rectifier potassium current (IK) in rapid pacing induced heart failure is lacking. Methods and results: Action potentials and whole-cell currents, IK, Ito1, IK1, and ICa-L were recorded in apical myocytes of left ventricle from 10 rabbits subjected to left ventricular pacing at 350–380 beats/min for 3–4 weeks and 10 controls with sham operation. Action potential duration at 90% repolarization (APD90) was prolonged in myocytes from failing hearts compared to controls at both cycle lengths of 333 and 1000 ms. Both E-4031-sensitive and -resistant components of IK (IKr, IKs) in myocytes from failing hearts were significantly less than those of control hearts; tail current densities of IKr and IKs following depolarization to +50 mV were 0.62±0.05 vs. 0.96±0.12 pA/pF (P<0.05), and 0.27±0.08 vs. 0.52±0.08 pA/pF (P<0.05), respectively. There was no significant difference between control and failing myocytes in the voltage- and time-dependence of activation of total IK, IKr and IKs. The peak of L-type Ca2+ current (ICa-L) was significantly reduced in myocytes from failing hearts (at +10 mV, –9.29±0.52 vs. –12.28±1.63 pA/pF, P<0.05), as was the Ca2+-independent transient outward current (Ito1; at +40 mV, 4.8±0.9 vs. 9.6±1.3 pA/pF, P<0.05). Steady state I–V curve for IK1 was similar in myocytes from failing and control hearts. Conclusions: Decrease of IK (both IKr and IKs) in addition to reduced Ito1, may underly action potential prolongation at physiological cycle length and thereby contribute to arrhythmogenesis in heart failure.
KEYWORDS Arrhythmia (mechanisms); Heart failure; Membrane currents; K-channel
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