S-nitrosylation of cardiac ion channels

Daniel R. Gonzalez, Adriana Treuer, Qi An Sun, Jonathan S. Stamler, Joshua M. Hare

Research output: Contribution to journalReview articlepeer-review

101 Scopus citations


Nitric oxide (NO) exerts ubiquitous signaling via posttranslational modification of cysteine residues, a reaction termed S-nitrosylation. Important substrates of S-nitrosylation that influence cardiac function include receptors, enzymes, ion channels, transcription factors, and structural proteins. Cardiac ion channels subserving excitation-contraction coupling are potentially regulated by S-nitrosylation. Specificity is achieved in part by spatial colocalization of ion channels with nitric oxide synthases (NOSs), enzymatic sources of NO in biologic systems, and by coupling of NOS activity to localized calcium/second messenger concentrations. Ion channels regulate cardiac excitability and contractility in millisecond timescales, raising the possibility that NO-related species modulate heart function on a beat-to-beat basis. This review focuses on recent advances in understanding of NO regulation of the cardiac action potential and of the calcium release channel ryanodine receptor, which is crucial for the generation of force. S-Nitrosylation signaling is disrupted in pathological states in which the redox state of the cell is dysregulated, including ischemia, heart failure, and atrial fibrillations.

Original languageEnglish (US)
Pages (from-to)188-195
Number of pages8
JournalJournal of Cardiovascular Pharmacology
Issue number3
StatePublished - Sep 2009


  • Heart
  • Nitric oxide
  • Nitrosylation
  • Oxidation
  • Ryanodine receptor

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine


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