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Updated: Jul 14, 2026

Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
Expression and function of ATP-dependent potassium channels in late post-infarction remodeling
Nadia Isidoro Tavares1, Pierre Philip-Couderc, Irène Papageorgiou
1Division of Cardiology, Geneva University Hospitals, 24 Micheli-du-Crest, 1211 Geneva 14, Switzerland.
After heart attack, altered ATP-dependent potassium (KATP) channels in remodeled heart muscle contribute to dangerous arrhythmias. Activating these channels may prevent fatal heart rhythms in heart failure patients.
Area of Science:
- Cardiology
- Molecular Biology
- Electrophysiology
Background:
- Myocardial remodeling post-infarction increases fatal arrhythmia risk.
- Heterogeneous action potential prolongation in surviving heart cells is a key factor.
- Sarcolemmal ATP-dependent potassium (KATP) channels regulate cardiomyocyte electrical activity.
Purpose of the Study:
- To investigate the role of KATP channels in action potential heterogeneity after myocardial infarction.
- To determine if KATP channels generate or prevent action potential prolongation.
Main Methods:
- Isolated cardiomyocytes from infarct border zone, septum, and right ventricle of rat hearts 20 weeks post-coronary occlusion.
- Assessed expression of KATP channel subunits (Kir6.1, Kir6.2, SUR).
- Measured KATP current and action potential duration, including response to diazoxide.
Main Results:
- Increased Kir6.1 and SUR subunit expression in infarct border zone cardiomyocytes.
- Significant action potential prolongation in infarct border zone myocytes (74 ms vs. 41 ms sham).
- Diazoxide activation of KATP channels normalized action potential duration in remodeled myocytes (to 42 ms).
Conclusions:
- Remodeled myocardium post-infarction exhibits heterogeneous alterations in KATP channel expression and function.
- These KATP channel changes correlate with action potential prolongation heterogeneity.
- Selective activation of diazoxide-sensitive KATP channels is a potential therapeutic strategy for post-infarction arrhythmias.
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