The NO cascade, eNOS location, and microvascular permeability

Walter N. Durán, Jerome W. Breslin, Fabiola A. Sánchez

Research output: Contribution to journalReview article

114 Scopus citations

Abstract

The nitric oxide (NO) cascade and endothelial NO synthase (eNOS) are best known for their role in endothelium-mediated relaxation of vascular smooth muscle. Activation of eNOS by certain inflammatory stimuli and enhanced NO release have also been shown to promote increased microvascular permeability. However, it is not entirely clear why activation of eNOS by certain vasodilatory agents, like acetylcholine, does not affect microvascular permeability, whereas activation of eNOS by other inflammatory agents that increase permeability, like platelet-activating factor, does not cause vasodilation. In this review, we discuss the evidence demonstrating the role of eNOS in the elevation of microvascular permeability. We also examine the relative importance of eNOS phosphorylation and localization in its function to promote elevated microvascular permeability as well as emerging topics with regard to eNOS and microvascular permeability regulation.

Original languageEnglish (US)
Pages (from-to)254-261
Number of pages8
JournalCardiovascular research
Volume87
Issue number2
DOIs
StatePublished - Jul 2010

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Keywords

  • Endothelial nitric oxide synthase
  • Inflammation
  • Microvascular permeability
  • Protein traffic

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