Oxidative modification of ion channel activity of ryanodine receptor

Antioxid Redox Signal. 2000 Spring;2(1):35-40. doi: 10.1089/ars.2000.2.1-35.

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium Signaling / drug effects*
  • Calcium Signaling / physiology
  • Carrier Proteins*
  • Cysteine / metabolism
  • Cystine / metabolism
  • Hydrogen Peroxide / pharmacology
  • Hydroxyl Radical / pharmacology
  • Ion Transport / drug effects
  • Lipid Bilayers
  • Models, Biological
  • Muscle Proteins / chemistry
  • Muscle Proteins / drug effects*
  • Muscle Proteins / metabolism
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / ultrastructure
  • Myocardium / metabolism
  • Myocardium / ultrastructure
  • Nitric Oxide / pharmacology
  • Nitroso Compounds / pharmacology
  • Oxidants / pharmacology
  • Oxidation-Reduction
  • Protein Conformation / drug effects
  • Rabbits
  • Reducing Agents / pharmacology
  • Ryanodine Receptor Calcium Release Channel / chemistry
  • Ryanodine Receptor Calcium Release Channel / drug effects*
  • Ryanodine Receptor Calcium Release Channel / metabolism
  • Sarcoplasmic Reticulum / drug effects*
  • Sarcoplasmic Reticulum / metabolism
  • Sulfhydryl Compounds / metabolism

Substances

  • Carrier Proteins
  • Lipid Bilayers
  • Muscle Proteins
  • Nitroso Compounds
  • Oxidants
  • Reducing Agents
  • Ryanodine Receptor Calcium Release Channel
  • Sulfhydryl Compounds
  • triadin
  • Nitric Oxide
  • Hydroxyl Radical
  • Cystine
  • Hydrogen Peroxide
  • Cysteine