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Am J Physiol Heart Circ Physiol 276: H98-H106, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 1, H98-H106, January 1999

Transmembrane ICa contributes to rate-dependent changes of action potentials in human ventricular myocytes

Gui-Rong Li1, Baofeng Yang1, Jianlin Feng1, Ralph F. Bosch1, Michel Carrier2, and Stanley Nattel1,3

Departments of 1 Medicine and 2 Surgery, Montreal Heart Institute and University of Montreal, and 3 Department of Pharmacology, McGill University, Montreal, Quebec, Canada H1T 1C8

The mechanism of action potential abbreviation caused by increasing rate in human ventricular myocytes is unknown. The present study was designed to determine the potential role of Ca2+ current (ICa) in the rate-dependent changes in action potential duration (APD) in human ventricular cells. Myocytes isolated from the right ventricle of explanted human hearts were studied at 36°C with whole cell voltage and current-clamp techniques. APD at 90% repolarization decreased by 36 ± 4% when frequency increased from 0.5 to 2 Hz. Equimolar substitution of Mg2+ for Ca2+ significantly decreased rate-dependent changes in APD (to 6 ± 3%, P < 0.01). Peak ICa was decreased by 34 ± 3% from 0.5 to 2 Hz (P < 0.01), and ICa had recovery time constants of 65 ± 12 and 683 ± 39 ms at -80 mV. Action potential clamp demonstrated a decreasing contribution of ICa during the action potential as rate increased. The rate-dependent slow component of the delayed rectifier K+ current (IKs) was not observed in four cells with an increase in frequency from 0.5 to 3.3 Hz, perhaps because the IKs is so small that the increase at a high rate could not be seen. These results suggest that reduction of Ca2+ influx during the action potential accounts for most of the rate-dependent abbreviation of human ventricular APD.

calcium current; ion channels; action potential; electrophysiology; cardiac arrhythmias


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