Interaction between nitric oxide signaling and gap junctions: effects on vascular function

Biochim Biophys Acta. 2012 Aug;1818(8):1895-902. doi: 10.1016/j.bbamem.2011.07.031. Epub 2011 Jul 28.

Abstract

Nitric oxide signaling, through eNOS (or possibly nNOS), and gap junction communication are essential for normal vascular function. While each component controls specific aspects of vascular function, there is substantial evidence for cross-talk between nitric oxide signaling and the gap junction proteins (connexins), and more recently, protein-protein association between eNOS and connexins. This review will examine the evidence for interaction between these pathways in normal and diseased arteries, highlight the questions that remain about the mechanisms of their interaction, and explore the possible interaction between nitric oxide signaling and the newly discovered pannexin channels. This article is part of a Special Issue entitled: The Communicating junctions, composition, structure and characteristics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Atherosclerosis / metabolism
  • Caveolin 1 / metabolism
  • Cells, Cultured
  • Connexins / metabolism
  • Cyclic GMP / metabolism
  • Diabetes Mellitus / metabolism
  • Gap Junctions / metabolism
  • Gap Junctions / physiology*
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Hypertension / metabolism
  • Mice
  • Models, Biological
  • Nerve Tissue Proteins / metabolism
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type III / metabolism
  • Protein Binding
  • Signal Transduction

Substances

  • Caveolin 1
  • Connexins
  • Nerve Tissue Proteins
  • PANX1 protein, human
  • Nitric Oxide
  • Nitric Oxide Synthase Type III
  • Cyclic GMP