© 2004 Society for Research on Nicotine and Tobacco
L-Arginine prevents impaired endothelium-dependent cerebral arteriolar dilatation during acute infusion of nicotine
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center Omaha, NE
Correspondence: William G. Mayhan, Ph.D., Department of Cellular and Integrative Physiology, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA. Tel.: +1 (402)-559-5329; Fax: +1 (402)-559-4438; E-mail: wgmayhan{at}unmc.edu
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Abstract |
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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 (10–3 M). 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.
Received: February 17, 2003; Accepted: July 2, 2003
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