Abstract
The ryanodine receptor (RyR) is involved in the physiological Ca2+ release from the sarcoplasmic reticulum in both skeletal and cardiac muscles. The redox regulation is a plausible endogenous regulatory mechanism of the RyR. Sulfhydryl oxidation or S-nitrosylation of the cardiac RyR has been reported to activate the channel. Our laboratory demonstrated that hydroxyl radicals also activate the cardiac Ca2+-release channel activity, likely through the modification of sulfhydryl groups of the RyR.
MeSH terms
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Animals
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Calcium Signaling / drug effects*
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Calcium Signaling / physiology
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Carrier Proteins*
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Cysteine / metabolism
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Cystine / metabolism
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Hydrogen Peroxide / pharmacology
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Hydroxyl Radical / pharmacology
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Ion Transport / drug effects
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Lipid Bilayers
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Models, Biological
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Muscle Proteins / chemistry
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Muscle Proteins / drug effects*
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Muscle Proteins / metabolism
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Muscle, Skeletal / metabolism
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Muscle, Skeletal / ultrastructure
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Myocardium / metabolism
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Myocardium / ultrastructure
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Nitric Oxide / pharmacology
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Nitroso Compounds / pharmacology
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Oxidants / pharmacology
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Oxidation-Reduction
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Protein Conformation / drug effects
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Rabbits
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Reducing Agents / pharmacology
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Ryanodine Receptor Calcium Release Channel / chemistry
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Ryanodine Receptor Calcium Release Channel / drug effects*
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Ryanodine Receptor Calcium Release Channel / metabolism
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Sarcoplasmic Reticulum / drug effects*
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Sarcoplasmic Reticulum / metabolism
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Sulfhydryl Compounds / metabolism
Substances
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Carrier Proteins
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Lipid Bilayers
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Muscle Proteins
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Nitroso Compounds
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Oxidants
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Reducing Agents
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Ryanodine Receptor Calcium Release Channel
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Sulfhydryl Compounds
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triadin
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Nitric Oxide
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Hydroxyl Radical
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Cystine
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Hydrogen Peroxide
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Cysteine