Inhibition of agonist-induced vasocontraction and impairment of endothelium-dependent vasorelaxation by extract of motorcycle exhaust particles in vitro

Yu Wen Cheng, Jaw Jou Kang

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The in vitro effects of motorcycle exhaust particulate extract (MEPE) on blood vessels were studied in thoracic aorta isolated from Wistar rat. The MEPE relaxed the phenylephrine-precontracted aorta with an EC50 value of 0.05 ± 0.004 mg/ml. This relaxing effect of MEPE persisted in endothelium-denuded aorta, suggesting that the relaxation induced by MEPE is endothelium-independent. The phenylephrine-induced vasocontraction and inositol 1,4,5-triphosphate formation were inhibited concentration dependently in aorta pretreated with MEPE. However, the high-K+-induced vasocontraction and the Ca2+ sensitivity of the contractile proteins were not significantly affected by MEPE. In addition to the inhibitory effects on agonist-induced contraction, the vasorelaxing effects both of acetylcholine and of sodium nitroprusside were impaired by MEPE. The inhibitory effects of MEPE on acetylcholine and sodium nitroprusside, but not phenylephrine, were reversed by cotreatment with superoxide dismutase. These results showed that the MEPE, added in vitro, inhibited the phenylephrine-induced, but not depolarization-induced, vasocontraction of aorta. The MEPE also impaired the vasorelaxation induced by acetylcholine in a superoxide anion-dependent manner.

Original languageEnglish
Pages (from-to)75-87
Number of pages13
JournalJournal of Toxicology and Environmental Health - Part A
Volume57
Issue number2
Publication statusPublished - May 28 1999
Externally publishedYes

Fingerprint

Motorcycles
Vasodilation
Endothelium
Phenylephrine
Aorta
Acetylcholine
Nitroprusside
Sodium
sodium
In Vitro Techniques
motorcycle
particle
Contractile Proteins
Inositol 1,4,5-Trisphosphate
Depolarization
Blood vessels
Thoracic Aorta
Superoxides
contraction
Superoxide Dismutase

ASJC Scopus subject areas

  • Environmental Science(all)
  • Environmental Chemistry
  • Public Health, Environmental and Occupational Health
  • Pollution
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

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title = "Inhibition of agonist-induced vasocontraction and impairment of endothelium-dependent vasorelaxation by extract of motorcycle exhaust particles in vitro",
abstract = "The in vitro effects of motorcycle exhaust particulate extract (MEPE) on blood vessels were studied in thoracic aorta isolated from Wistar rat. The MEPE relaxed the phenylephrine-precontracted aorta with an EC50 value of 0.05 ± 0.004 mg/ml. This relaxing effect of MEPE persisted in endothelium-denuded aorta, suggesting that the relaxation induced by MEPE is endothelium-independent. The phenylephrine-induced vasocontraction and inositol 1,4,5-triphosphate formation were inhibited concentration dependently in aorta pretreated with MEPE. However, the high-K+-induced vasocontraction and the Ca2+ sensitivity of the contractile proteins were not significantly affected by MEPE. In addition to the inhibitory effects on agonist-induced contraction, the vasorelaxing effects both of acetylcholine and of sodium nitroprusside were impaired by MEPE. The inhibitory effects of MEPE on acetylcholine and sodium nitroprusside, but not phenylephrine, were reversed by cotreatment with superoxide dismutase. These results showed that the MEPE, added in vitro, inhibited the phenylephrine-induced, but not depolarization-induced, vasocontraction of aorta. The MEPE also impaired the vasorelaxation induced by acetylcholine in a superoxide anion-dependent manner.",
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AU - Kang, Jaw Jou

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N2 - The in vitro effects of motorcycle exhaust particulate extract (MEPE) on blood vessels were studied in thoracic aorta isolated from Wistar rat. The MEPE relaxed the phenylephrine-precontracted aorta with an EC50 value of 0.05 ± 0.004 mg/ml. This relaxing effect of MEPE persisted in endothelium-denuded aorta, suggesting that the relaxation induced by MEPE is endothelium-independent. The phenylephrine-induced vasocontraction and inositol 1,4,5-triphosphate formation were inhibited concentration dependently in aorta pretreated with MEPE. However, the high-K+-induced vasocontraction and the Ca2+ sensitivity of the contractile proteins were not significantly affected by MEPE. In addition to the inhibitory effects on agonist-induced contraction, the vasorelaxing effects both of acetylcholine and of sodium nitroprusside were impaired by MEPE. The inhibitory effects of MEPE on acetylcholine and sodium nitroprusside, but not phenylephrine, were reversed by cotreatment with superoxide dismutase. These results showed that the MEPE, added in vitro, inhibited the phenylephrine-induced, but not depolarization-induced, vasocontraction of aorta. The MEPE also impaired the vasorelaxation induced by acetylcholine in a superoxide anion-dependent manner.

AB - The in vitro effects of motorcycle exhaust particulate extract (MEPE) on blood vessels were studied in thoracic aorta isolated from Wistar rat. The MEPE relaxed the phenylephrine-precontracted aorta with an EC50 value of 0.05 ± 0.004 mg/ml. This relaxing effect of MEPE persisted in endothelium-denuded aorta, suggesting that the relaxation induced by MEPE is endothelium-independent. The phenylephrine-induced vasocontraction and inositol 1,4,5-triphosphate formation were inhibited concentration dependently in aorta pretreated with MEPE. However, the high-K+-induced vasocontraction and the Ca2+ sensitivity of the contractile proteins were not significantly affected by MEPE. In addition to the inhibitory effects on agonist-induced contraction, the vasorelaxing effects both of acetylcholine and of sodium nitroprusside were impaired by MEPE. The inhibitory effects of MEPE on acetylcholine and sodium nitroprusside, but not phenylephrine, were reversed by cotreatment with superoxide dismutase. These results showed that the MEPE, added in vitro, inhibited the phenylephrine-induced, but not depolarization-induced, vasocontraction of aorta. The MEPE also impaired the vasorelaxation induced by acetylcholine in a superoxide anion-dependent manner.

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