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Endothelial‐derived microparticles inhibit pulmonary artery vasodilation
Author(s) -
Peterson Danielle B.,
Kaul Sushma,
Wang Jingli,
Jones Deron W.,
Oldham Keith T.,
Pritchard Kirkwood A.,
Sander Tara
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.329.11
Subject(s) - vasodilation , pulmonary artery , medicine , acetylcholine , endothelium , lung , pharmacology , endothelial stem cell , cardiology , chemistry , in vitro , biochemistry
Endothelial‐derived microparticles (EMPs) are produced by endothelial cells in response to cell injury, activation and apoptosis. Elevated plasma concentrations of EMPs are associated with a variety of vascular and inflammatory diseases, including acute lung injury (ALI). However, the mechanisms by which EMPs contribute to pulmonary disease are unclear. We hypothesize that EMPs contribute to ALI by inhibiting endothelium‐mediated vasodilation in the pulmonary vasculature. To test this hypothesis, acetylcholine (ACh)‐mediated vasodilation was quantified using isolated thoracic aorta (TA) and pulmonary artery (PA) rings of C57BL/6 mice in the presence or absence of EMPs (20 K or 100 K EMPs/ml). Concentration dependent inhibition of ACh‐mediated vasodilation was observed for both TA and PA rings; furthermore, PA rings are more sensitive to the inhibitory effects of EMPs. In conclusion, EMPs attenuate endothelium‐mediated vasodilation at pathophysiologically relevant concentrations. EMPs also act in a tissue specific manner affecting the pulmonary vasculature disproportionate to other vascular beds. These data suggest that EMP damage to pulmonary endothelial cells may contribute to ALI. Funding provided by the Children's Research Institute and MCW Department of Surgery.