Superoxide dismutase restores endothelium-dependent arteriolar dilatation during acute infusion of nicotine

William G. Mayhan, Glenda M. Sharpe

Research output: Contribution to journalArticlepeer-review

45 Scopus citations

Abstract

We previously showed [Am. J. Physiol. 272 (Heart Circ. Physiol. 41): H2337-H2342, 1997] that nicotine impairs endothelium-dependent arteriolar dilatation. However, mechanisms that accounted for the effect of nicotine on endothelium-dependent vasodilatation were not examined. Thus the goal of this study was to examine the role of oxygen radicals in nicotine-induced impairment of arteriolar reactivity. We measured diameter of cheek pouch resistance arterioles (~50 μm diameter) in response to endothelium- dependent (ACh and ADP) and -independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine in the absence or presence of superoxide dismutase. ACh, ADP, and nitroglycerin produced dose-related dilatation of cheek pouch arterioles before infusion of vehicle or nicotine. Infusion of vehicle, in the absence or presence of superoxide dismutase (150 U/ml), did not alter endothelium-dependent or -independent arteriolar dilatation. In contrast, infusion of nicotine (2 μg · kg-1 min-1) impaired endothelium-dependent, but not -independent, arteriolar dilatation. In addition, the effect of nicotine on endothelium-dependent vasodilatation was reversed by topical application of superoxide dismutase. We suggest that nicotine impairs endothelium-dependent arteriolar dilatation via an increase in the synthesis/release of oxygen-derived free radicals.

Original languageEnglish (US)
Pages (from-to)1292-1298
Number of pages7
JournalJournal of Applied Physiology
Volume85
Issue number4
DOIs
StatePublished - Oct 1998

Keywords

  • Acetylcholine
  • Adenosine 5'-diphosphate
  • Cheek pouch
  • Endothelium-derived relaxing factor
  • Hamsters
  • Nitroglycerin
  • Oxygen radicals
  • Smoking

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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