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Ultrafine particulate matter exposure attenuates mouse aortic relaxations
Author(s) -
Wingard Christopher J,
Cozzi Emily,
Tuttle Brian,
Cascio Wayne E,
Devlin Robert B,
Lust Robert M,
Van Scott Michael R
Publication year - 2006
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.20.4.a293
Subject(s) - phenylephrine , adenosine , acetylcholine , medicine , endocrinology , endothelial dysfunction , aorta , chemistry , blood pressure
Particulate air pollution (PM) contributes to adverse cardiovascular events by yet unknown mechanisms. We tested the hypothesis that PM exposure altered endothelial regulation of systemic vascular tone. 6–10 week old male ICR mice were exposed to a single dose of 10, 30 or 100 μg of ultrafine PM or vehicle by intratracheal instillation. 24 hours later aortas were isolated and exposed to phenylephrine (PE), acetylcholine (ACH) or adenosine to probe their vascular responses. Constrictor responses to PE were not different between PM exposed and control aortas. PM exposure attenuated ACH relaxation in a dose‐dependent manner.In endothelial‐denuded aortas PM exposure increased the maximal contractile response (mN/mm 2 ) to 10μM adenosine (control 1.39 ± 0.02 vs. PM‐exposed 1.79 ± 0.11*). These results indicate that PM exposure altered endothelial‐dependent and independent vascular responsiveness and may contribute to cardiovascular complications. This abstract dose not necessarily represents EPA policy. Supported by Phillip Morris Foundation # 567881.