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Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor.

Publication ,  Journal Article
Li, Z; Carter, JD; Dailey, LA; Huang, Y-CT
Published in: Environ Health Perspect
August 2005

Exposure to particulate matter (PM) is associated with acute cardiovascular mortality and morbidity, but the mechanisms are not entirely clear. In this study, we hypothesized that PM may activate the angiotensin type 1 receptor (AT1R), a G protein-coupled receptor that regulates inflammation and vascular function. We investigated the acute effects of St. Louis, Missouri, urban particles (UPs; Standard Reference Material 1648) on the constriction of isolated rat pulmonary artery rings and the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 mitogen-activated protein kinases (MAPKs) in human pulmonary artery endothelial cells with or without losartan, an antagonist of AT1R. UPs at 1-100 microg/mL induced acute vasoconstriction in pulmonary artery. UPs also produced a time- and dose-dependent increase in phosphorylation of ERK1/2 and p38 MAPK. Losartan pretreatment inhibited both the vasoconstriction and the activation of ERK1/2 and p38. The water-soluble fraction of UPs was sufficient for inducing ERK1/2 and p38 phosphorylation, which was also losartan inhibitable. Copper and vanadium, two soluble transition metals contained in UPs, induced pulmonary vasoconstriction and phosphorylation of ERK1/2 and p38, but only the phosphorylation of p38 was inhibited by losartan. The UP-induced activation of ERK1/2 and p38 was attenuated by captopril, an angiotensin-converting enzyme inhibitor. These results indicate that activation of the local renin-angiotensin system may play an important role in cardiovascular effects induced by PM.

Duke Scholars

Published In

Environ Health Perspect

DOI

ISSN

0091-6765

Publication Date

August 2005

Volume

113

Issue

8

Start / End Page

1009 / 1014

Location

United States

Related Subject Headings

  • p38 Mitogen-Activated Protein Kinases
  • Vasoconstriction
  • Vanadium
  • Toxicology
  • Receptor, Angiotensin, Type 1
  • Rats, Sprague-Dawley
  • Rats
  • Pulmonary Artery
  • Phosphorylation
  • Particle Size
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Li, Z., Carter, J. D., Dailey, L. A., & Huang, Y.-C. (2005). Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor. Environ Health Perspect, 113(8), 1009–1014. https://doi.org/10.1289/ehp.7736
Li, Zhuowei, Jacqueline D. Carter, Lisa A. Dailey, and Yuh-Chin T. Huang. “Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor.Environ Health Perspect 113, no. 8 (August 2005): 1009–14. https://doi.org/10.1289/ehp.7736.
Li Z, Carter JD, Dailey LA, Huang Y-CT. Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor. Environ Health Perspect. 2005 Aug;113(8):1009–14.
Li, Zhuowei, et al. “Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor.Environ Health Perspect, vol. 113, no. 8, Aug. 2005, pp. 1009–14. Pubmed, doi:10.1289/ehp.7736.
Li Z, Carter JD, Dailey LA, Huang Y-CT. Pollutant particles produce vasoconstriction and enhance MAPK signaling via angiotensin type I receptor. Environ Health Perspect. 2005 Aug;113(8):1009–1014.

Published In

Environ Health Perspect

DOI

ISSN

0091-6765

Publication Date

August 2005

Volume

113

Issue

8

Start / End Page

1009 / 1014

Location

United States

Related Subject Headings

  • p38 Mitogen-Activated Protein Kinases
  • Vasoconstriction
  • Vanadium
  • Toxicology
  • Receptor, Angiotensin, Type 1
  • Rats, Sprague-Dawley
  • Rats
  • Pulmonary Artery
  • Phosphorylation
  • Particle Size