L-Arginine prevents impaired endothelium-dependent cerebral arteriolar dilatation during acute infusion of nicotine

Qin Fang, Hong Sun, William G. Mayhan

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Exogenous treatment with L-arginine has been shown to restore impaired nitric oxide synthase (NOS)-dependent dilatation of peripheral blood vessels during disease states. We have shown that nicotine impairs NOS-dependent arteriolar dilatation in the cerebral circulation. However, the role of L-arginine in impaired responses of cerebral arterioles during infusion of nicotine has not been examined. Thus the goal of the present study was to examine the role of L-arginine in nicotine-induced impairment of cerebral arteriolar reactivity. We measured the diameter of pial arterioles in response to NOS-dependent (5′-adenosine diphosphate [ADP] and acetylcholine) and NOS-independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine (2 μg/kg/min intravenously for 30 min followed by a maintenance dose of 0.35 μg/kg/min) in the absence or presence of L-arginine (10-3M). We found that topical application of L-arginine to cerebral microvessels during infusion of nicotine could prevent impaired NOS-dependent vasodilatation. We suggest that exogenous L-arginine may have a beneficial role in preventing cerebral microvascular dysfunction during exposure to nicotine.

Original languageEnglish (US)
Pages (from-to)1009-1014
Number of pages6
JournalNicotine and Tobacco Research
Volume6
Issue number6
DOIs
StatePublished - Dec 2004

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health

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