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A chloride current component induced by hypertrophy in rat ventricular myocytes
J P Bénitah1, A M Gómez, C Delgado
1Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore 21205, USA.
The American Journal of Physiology
|May 1, 1997
Summary
Hypertrophied rat heart cells develop a new chloride (Cl-) current component. This current component may shorten action potential duration, potentially protecting against cardiac arrhythmias.
Area of Science:
- Cardiovascular Physiology
- Cardiac Electrophysiology
- Molecular Cardiology
Background:
- Cardiac hypertrophy alters myocyte electrophysiology.
- Changes in membrane currents contribute to arrhythmogenesis in hypertrophied hearts.
Purpose of the Study:
- Investigate the impact of hypertrophy on membrane currents in rat ventricular myocytes.
- Identify novel currents contributing to altered electrophysiology in cardiac hypertrophy.
Main Methods:
- Whole-cell voltage-clamp technique on rat left ventricular myocytes.
- Analysis of current density-voltage relationships.
- Assessment of ion selectivity and pharmacological block (Ba2+, 9-AC).
Main Results:
- Increased slope of time-independent current density-voltage relationship in hypertrophied cells.
- Inward rectifier K+ current (Ba2+-sensitive) remained unchanged.
- A novel outwardly rectifying, Ba2+-resistant current was identified in hypertrophied cells.
- This current demonstrated sensitivity to extracellular Cl- concentration and partial block by 9-AC, suggesting a Cl- component.
- 9-AC prolonged action potentials in hypertrophied cells but not control cells.
Conclusions:
- A Cl- current component develops in hypertrophied rat heart cells.
- This newly developed Cl- current may shorten action potential duration.
- The identified Cl- current might play a protective role against cardiac arrhythmias in hypertrophy.