Opening of mitochondrial K(ATP) channels attenuates the ouabain-induced calcium overload in mitochondria
Autor: | Yuki Hirota, Toshiaki Sato, Hiroe Nakazawa, Chokoh Genka, Hideyuki Ishida, Haruaki Nakaya |
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Rok vydání: | 2001 |
Předmět: |
medicine.medical_specialty
Potassium Channels Physiology Heart Ventricles Mitochondrion Biology Ouabain Mitochondria Heart Adenosine Triphosphate Internal medicine medicine Diazoxide Myocyte Animals Channel blocker Enzyme Inhibitors Calcium overload Cells Cultured Fluorescent Dyes Membrane potential Microscopy Video Myocardium Membrane Proteins Depolarization Rats Endocrinology Microscopy Fluorescence Calcium Cardiology and Cardiovascular Medicine Hydroxy Acids Decanoic Acids medicine.drug |
Zdroj: | Circulation research. 89(10) |
ISSN: | 1524-4571 |
Popis: | We tested whether opening of mitochondrial ATP-sensitive K + (mitoK ATP ) channels depolarizes mitochondrial membrane potential (ΔΨ m ) and thereby prevents the mitochondrial Ca 2+ overload. With the use of a Nipkow disk confocal system, the mitochondrial Ca 2+ concentration ([Ca 2+ ] m ) and ΔΨ m in rat ventricular myocytes were measured by loading cells with Rhod-2 and JC-1, respectively. Exposure to ouabain (1 mmol/L) for 30 minutes produced mitochondrial Ca 2+ overload, and the intensity of Rhod-2 fluorescence significantly increased to 173±16% of baseline ( P ATP channel opener diazoxide (100 μmol/L) blunted the ouabain-induced mitochondrial Ca 2+ overload (131±10% of baseline; P m and reduced the intensity of JC-1 fluorescence during application of ouabain to 89±2% of baseline ( P ATP channel blocker 5-hydroxydecanoate (500 μmol/L). These results indicate that opening of mitoK ATP channels prevents a mitochondrial Ca 2+ overload in association with ΔΨ m depolarization and thereby protects myocardium against ischemic damage. |
Databáze: | OpenAIRE |
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