Journal
CARDIOVASCULAR RESEARCH
Volume 87, Issue 2, Pages 254-261Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvq139
Keywords
Endothelial nitric oxide synthase; Microvascular permeability; Inflammation; Protein traffic
Categories
Funding
- National Institutes of Health [5RO1 HL070634-07, 5RO1 HL088479-02, 5P20 RR01876-07]
- American Heart Association
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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.
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