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Articles in PresS, published online ahead of print October 10, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00752.2002
Submitted on August 29, 2002
Accepted on October 3, 2002
1 Physiology, University of Nebraska Medical Center, Omaha, NE, USA
* To whom correspondence should be addressed. E-mail: wgmayhan{at}unmc.edu.
The effects of nicotine on NOS-dependent reactivity of cerebral arterioles remain uncertain. Our first goal was to examine whether infusion of nicotine alters NOS-dependent reactivity of cerebral arterioles. Our second goal was to examine mechanisms that may account for the effects of nicotine on cerebral arterioles. We measured diameter of pial arterioles to NOS-dependent (5’-adenosine diphosphate (ADP) and acetylcholine) and -independent (nitroglycerin) agonists before and after infusion of nicotine (2µg/kg/min iv for 30 min followed by a maintenance dose of 0.35µg/kg/min). ADP- and acetylcholine-induced vasodilatation was impaired following infusion of nicotine. In contrast, nicotine did not alter vasodilatation to nitroglycerin. Next, we examined whether impaired responses of pial arterioles during infusion of nicotine may be related to oxygen radicals. We found that application of superoxide dismutase or tetrahydrobiopterin during infusion of nicotine could prevent impaired NOSdependent vasodilatation. Thus, acute exposure of cerebral vessels to nicotine specifically impairs NOS-dependent dilatation via the production of oxygen radicals possibly related to an alteration in the utilization of tetrahydrobiopterin.
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