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Received February 25, 2002
Accepted after revision March 5, 2002
1 Department of Cardiology of the First Affiliated Hospital to Suzhou University, Suzhou Jiangsu 215006, People's Republic of China
2 Cell Biology and Anatomy, University of Miami, School of Medicine, Miami, FL 33136, USA
3 Department of Molecular and Cellular Pharmacology, University of Miami, School of Medicine, Miami, FL 33136, USA
4 Department of Pediatrics, University of Miami, School of Medicine, Miami, FL 33136, USA
5 Department of Medicine (Cardiology), University of Miami, School of Medicine, Miami, FL 33136, USA
6 Department of Molecular and Cellular Pharmacology (R-189), University of Miami School of Medicine, PO Box 016189, Miami, FL 33101, USA
* To whom correspondence should be addressed. E-mail: abassett{at}med.miami.edu.
The durations of transmembrane action potentials recorded from single myocytes isolated from the endocardial surface of hypertrophied left ventricles of rats were increased, compared to the durations recorded from normal left ventricular cells at 36-37 °C. Exposure to phalloidin (1-20 µM, < 20 min), a specific stabilizer of the non-myofibrillar actin microfilament component of the cardiac cytoskeleton, had no effect on action potential duration of normal cells, but significantly shortened the prolonged action potentials of hypertrophied cells. Cytochalasin D (5-50 µM), a disrupter of the actin microfilaments, also had little effect on action potential duration of normal cells. However, cytochalasin D further increased the action potential duration of hypertrophied cells at 10 min exposure. The addition of phalloidin to solutions containing cytochalasin D, reduced the latter's increase of action potential duration in hypertrophied cells. Whole-cell transient outward K+ current (Ito1) density was significantly decreased in hypertrophied cells. At a test potential of +60 mV, the mean Ito1 density recorded from normal cells was 13.5 ± 1.1 pA pF-1 (n = 18) compared to 4.17 ± 1.2 pA pF-1 for LVH cells (n = 22; P < 0.05). Phalloidin (20 µM) increased and cytochalasin D (50 µM) decreased whole-cell Ito1 in hypertrophied cells but had no effect on Ito1, in normal cells. When equimolar concentrations were used, phalloidin, 10 µM, reversed the decrease in Ito1 brought about by cytochalasin D, 10 µM, in hypertrophied cells. The calcium L-type current (ICa,L) density was reduced in LVH compared to normal cells. Phalloidin (20 µM) and cytochalasin D (50 µM) had no effect on ICa,L in normal or LVH myocytes. The decrease in Ito1 in hypertrophied cells and the altered Ito1 responsiveness to phalloidin and cytochalasin D reflect modification of Ito1 channel function mediated, in part, through hypertrophy-altered cytoskeletal actin microfilament regulation of Ito1.
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