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A novel anionic inward rectifier in native cardiac myocytes.
1Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557-0046, USA. dduan@med.unr.edu
Circulation Research
|March 4, 2000
Summary
Researchers identified a new chloride (Cl-) inward rectifier (I(Cl.ir)) in mammalian heart. This novel channel, likely ClC-2, plays a role in cardiac electrical activity and cell volume regulation.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Cationic inward rectifier channels (Kir, I(f)) are known in cardiac myocytes.
- Anionic inward rectifiers in the heart remain uncharacterized.
Purpose of the Study:
- To functionally and molecularly identify novel anionic inward rectifiers in the mammalian heart.
- To investigate the physiological role of these channels in cardiac function.
Main Methods:
- Electrophysiological recordings (whole-cell patch-clamp) in mouse and guinea pig cardiac myocytes.
- Pharmacological characterization of the identified current.
- Molecular identification using RT-PCR and Northern blot analysis for ClC-2 expression.
Main Results:
- A novel chloride (Cl-) inward rectifier current (I(Cl.ir)) was identified in mammalian cardiac myocytes.
- The current exhibited slow activation upon hyperpolarization and was sensitive to cell volume changes.
- I(Cl.ir) showed specific anion permeability (Cl- > I-) and was blocked by 9-anthracene-carboxylic acid and cadmium.
- Expression of ClC-2 chloride channels was confirmed in cardiac tissues and isolated myocytes.
Conclusions:
- A novel inward rectifying chloride current (I(Cl.ir)) is present in the mammalian heart.
- The properties are consistent with ClC-2 chloride channels.
- ClC-2 channels may be crucial for regulating cardiac electrical activity and cell volume.