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Rate-dependent changes in action potential duration and membrane currents in hamster ventricular myocytes
Ivan Kocic1, Yuji Hirano, Masayasu Hiraoka
1Department of Cardiovascular Diseases, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.
Pflugers Archiv : European Journal of Physiology
|January 26, 2002
Summary
Hamster hearts show action potential duration prolongation at faster rates, primarily due to slow recovery of the Ito1 current. This finding is crucial for understanding hamster models of cardiomyopathy.
Area of Science:
- Cardiovascular Physiology
- Electrophysiology
- Cardiac Ion Channels
Background:
- Hamsters are a common model for cardiomyopathy research.
- However, the detailed electrophysiological properties of the hamster heart remain unclear.
Purpose of the Study:
- To investigate rate-dependent changes in action potentials in hamster ventricular myocytes.
- To identify the underlying ionic mechanisms responsible for these changes.
Main Methods:
- Utilized the whole-cell patch clamp technique on isolated hamster ventricular myocytes.
- Examined action potential duration (APD) and ionic currents at various stimulation frequencies.
- Applied pharmacological agents like 4-aminopyridine (4-AP) and Cd2+ to probe ionic contributions.
Main Results:
- Action potential duration (APD) progressively prolonged with increasing stimulation rates up to 6.0 Hz.
- The slow component of inactivation recovery for the Ito1 current (980 ms) was significantly longer than for I(Ca,L) (20 ms).
- 4-aminopyridine (4-AP) markedly prolonged APD and abolished rate-dependent prolongation, while Cd2+ shortened APD.
Conclusions:
- The slow recovery from inactivation of the Ito1 current is the primary determinant of action potential duration prolongation at faster rates in hamster ventricular myocytes.
- These findings provide critical electrophysiological insights for utilizing hamsters as a model for cardiac diseases.