HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 100/2/631    most recent 00975.2005v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Fang, Q. Articles by Mayhan, W. G. Search for Related Content PubMed PubMed Citation Articles by Fang, Q. Articles by Mayhan, W. G.

Inhibition of NADPH oxidase improves impaired reactivity of pial arterioles during chronic exposure to nicotine

Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska

Submitted 10 August 2005 ; accepted in final form 4 October 2005

Our goals were to determine whether chronic exposure to nicotine alters nitric oxide synthase (NOS)-dependent reactivity of cerebral (pial) arterioles and to identify a potential role for NADPH oxidase in impaired NOS-dependent responses during chronic exposure to nicotine. We measured in vivo diameter of pial arterioles to NOS-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in saline-treated rats and rats chronically treated with nicotine (2 mg·kg^–1·day^–1 for 2 wk via an osmotic minipump). We found that NOS-dependent, but not -independent, vasodilatation was impaired in nicotine-treated compared with saline-treated rats. In addition, the production of superoxide anion (lucigenin chemiluminescence) was increased in rats treated with nicotine compared with saline-treated rats. Furthermore, using Western blot analysis, we found that chronic exposure to nicotine increased p47phox protein in the parietal cortex. Finally, we found that apocynin (40 mg·kg^–1·day^–1) in the drinking water to inhibit NADPH oxidase alleviated impaired NOS-dependent cerebral vasodilatation in nicotine treated rats but did not alter NOS-dependent responses in saline treated rats and did not alter NOS-independent reactivity in saline- or nicotine-treated rats. These findings suggest that chronic exposure to nicotine impairs NOS-dependent dilatation of pial arterioles by a mechanism that appears to be related to the formation of superoxide anion via activation of NADPH oxidase.

smoking; brain; nitric oxide; superoxide anion; apocynin

This article has been cited by other articles:

				R. H. Fabian, J. R. Perez-Polo, and T. A. Kent Perivascular nitric oxide and superoxide in neonatal cerebral hypoxia-ischemia Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1809 - H1814. [Abstract] [Full Text] [PDF]

				H. Iida, M. Iida, M. Takenaka, N. Fukuoka, and S. Dohi Rho-kinase inhibitor and Nicotinamide Adenine Dinucleotide PHosphate oxidase inhibitor prevent impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats Journal of Renin-Angiotensin-Aldosterone System, June 1, 2008; 9(2): 89 - 94. [Abstract] [PDF]

				D. M. Arrick and W. G. Mayhan Acute infusion of nicotine impairs nNOS-dependent reactivity of cerebral arterioles via an increase in oxidative stress J Appl Physiol, December 1, 2007; 103(6): 2062 - 2067. [Abstract] [Full Text] [PDF]