S-Nitrosylation of cardiac ion channels.


Journal Article (Review)

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 fibrillation.

Full Text

Duke Authors

Cited Authors

  • Gonzalez, DR; Treuer, A; Sun, Q-A; Stamler, JS; Hare, JM

Published Date

  • September 2009

Published In

Volume / Issue

  • 54 / 3

Start / End Page

  • 188 - 195

PubMed ID

  • 19687749

Pubmed Central ID

  • 19687749

Electronic International Standard Serial Number (EISSN)

  • 1533-4023

Digital Object Identifier (DOI)

  • 10.1097/FJC.0b013e3181b72c9f


  • eng

Conference Location

  • United States