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Am J Physiol Heart Circ Physiol 275: H1717-H1725, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 5, H1717-H1725, November 1998

Ultrarapid delayed rectifier current inactivation in human atrial myocytes: properties and consequences

Jianlin Feng1,2, Donghui Xu1,2, Zhiguo Wang1,2,3, and Stanley Nattel1,2,3,4

1 Department of Medicine and 2 Research Center, Montreal Heart Institute, Montreal H1T 1C8; 3 Department of Medicine, University of Montreal, Montreal H3C 3J7; and 4 Department of Pharmacology and Therapeutics, McGill University, Montreal H3G 1Y6, Quebec, Canada

The ultrarapid delayed rectifier current (IK,ur) plays a significant role in human atrial repolarization and is generally believed to show little rate dependence because of slow and partial inactivation. This study was designed to evaluate in detail the properties and consequences of IK,ur inactivation in isolated human atrial myocytes. IK,ur inactivated with a biexponential time course and a half-inactivation voltage of -7.5 ± 0.6 mV (mean ± SE), with complete inactivation during 50-s pulses to voltages positive to +10 mV (37°C). Recovery from inactivation proceeded slowly, with time constants of 0.42 ± 0.06 and 7.9 ± 0.9 s at -80 mV (37°C). Substantial frequency dependence was observed at 37°C over a clinically relevant range of frequencies. Inactivation was faster and occurred at more positive voltages at 37°C compared with room temperature. The voltage and time dependencies of Kv1.5 inactivation were studied in Xenopus oocytes to avoid overlapping currents and strongly resembled those of IK,ur in native myocytes. We conclude that, while IK,ur inactivation is slow, it is extensive, and slow recovery from inactivation confers important frequency dependence with significant consequences for understanding the role of IK,ur in human atrial repolarization.

potassium channels; action potentials; atrial fibrillation; cardiac electrophysiology; antiarrhythmic drugs


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