Ionic basis for membrane potential changes induced by hypoosmotic stress in guinea-pig ventricular myocytes
1Department of Cardiovascular Diseases and Etiology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Cardiovascular Research
|June 12, 2001
Summary
Hypoosmotic stress alters cardiac action potentials by activating specific ion currents, causing initial prolongation then shortening of action potential duration and resting potential changes in ventricular myocytes.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
Background:
- Hypoosmotic challenge significantly impacts cellular function.
- Understanding ionic current involvement in cardiac action potential changes is crucial.
Purpose of the Study:
- To investigate the causal relationship between action potential changes and ionic current activation during hypoosmotic stress.
- To elucidate the specific ionic currents responsible for observed electrophysiological alterations.
Main Methods:
- Whole-cell patch-clamp technique was employed to record membrane potentials and currents.
- Guinea-pig ventricular myocytes were subjected to controlled hypotonic stress (0.6 T).
Main Results:
- Hypotonic stress initially prolonged action potential duration at 90% repolarization (APD(90)) via non-selective cation (NSC) current activation.
- Later, APD(90) shortened, and resting potential (RP) depolarized due to increased slow component of delayed rectifier K(+) current (I(Ks)) and chloride channel (I(Clswell)) activation.
- RP depolarization was dependent on extracellular potassium concentration ([K(+)](o)).
Conclusions:
- The dynamic changes in APD(90) during hypoosmotic stress result from sequential activation of NSC, I(Ks), and I(Clswell) currents.
- Resting potential depolarization is likely caused by subsarcolemmal potassium dilution and/or altered ion permeability ratios.
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