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Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
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Elevated potassium outward currents in hyperoxia treated atrial cardiomyocytes.
Zhanna Vysotskaya1, Bojjibabu Chidipi1, Jennifer L Rodgers2
1Department of Molecular Pharmacology and Physiology, Morsani College of Medicine, University of South Florida, Tampa, Florida.
Journal of Cellular Physiology
|November 16, 2017
Summary
High oxygen therapy (hyperoxia) can cause atrial electrical remodeling in mice, increasing specific potassium currents and shortening action potential durations. This suggests hyperoxia impacts heart electrical function beyond the ventricles.
Area of Science:
- Cardiology
- Electrophysiology
- Critical Care Medicine
Background:
- Hyperoxia (100% oxygen) is common in intensive care units (ICUs).
- While beneficial for lung disorders, hyperoxia is linked to increased in-hospital mortality.
- Previous studies indicated hyperoxia causes ventricular remodeling.
Purpose of the Study:
- To investigate the effects of hyperoxia on atrial electrophysiology.
- To assess changes in specific potassium channel (Kv1.5, Kv4.2, KChIP2) expression.
- To determine if hyperoxia induces atrial electrical remodeling.
Main Methods:
- Whole-cell patch-clamp electrophysiology in mouse atrial cardiomyocytes.
- Real-time quantitative RT-PCR for gene expression analysis.
- Western blotting for protein level assessment.
Main Results:
- Hyperoxia (3 days) increased outward potassium currents, specifically ultrarapid delayed rectifier (IKur) and transient outward (Ito) currents.
- Action potential durations (APD) were significantly shortened in hyperoxia-exposed atria.
- Kv1.5 and KChIP2 transcript and protein levels were elevated, while Kv4.2 remained unchanged.
Conclusions:
- Hyperoxia induces significant electrical remodeling in atrial cardiomyocytes.
- Increased IKur and Ito contribute to altered atrial electrophysiology.
- Hyperoxia's cardiac effects extend to atrial remodeling, not just ventricular.
Keywords:
atriacardiomyocyteshyperoxiarapidly inactivating transient outward K+ current (Ito) arrhythmiasultrarapid delayed rectifier outward K+ current (IKur) rapidly activatingwhole-cell electrophysiologyMore Related Videos
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