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Adverse effects of cigarette smoke on NO bioavailability : role of arginine metabolism and oxidative stress

Zhang, Wei-Zheng, Venardos, Kylie, Chin-Dusting, Jaye and Kaye, David M. 2006, Adverse effects of cigarette smoke on NO bioavailability : role of arginine metabolism and oxidative stress, Hypertension, vol. 48, no. 2, pp. 278-285, doi: 10.1161/01.HYP.0000231509.27406.42.

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Title Adverse effects of cigarette smoke on NO bioavailability : role of arginine metabolism and oxidative stress
Author(s) Zhang, Wei-Zheng
Venardos, Kylie
Chin-Dusting, Jaye
Kaye, David M.
Journal name Hypertension
Volume number 48
Issue number 2
Start page 278
End page 285
Total pages 8
Publisher Lippincott Williams & Wilkins
Place of publication Philadelphia, Pa.
Publication date 2006-08
ISSN 0194-911X
1524-4563
Keyword(s) smoking
endothelium
metabolism
Summary Endothelial dysfunction is a hallmark of cardiovascular disease, and the l-arginine:NO pathway plays a critical role in determining endothelial function. Recent studies suggest that smoking, a well-recognized risk factor for vascular disease, may interfere with l-arginine and NO metabolism; however, this remains poorly characterized. Accordingly, we performed a series of complementary in vivo and in vitro studies to elucidate the mechanism by which cigarette smoke adversely affects endothelial function. In current smokers, plasma levels of asymmetrical dimethyl-arginine (ADMA) were 80% higher (P=0.01) than nonsmokers, whereas citrulline (17%; P<0.05) and N-hydroxy-l-arginine (34%; P<0.05) were significantly lower. Exposure to 10% cigarette smoke extract (CSE) significantly affected endothelial arginine metabolism with reductions in the intracellular content of citrulline (81%), N-hydroxy-l-arginine (57%), and arginine (23%), while increasing ADMA (129%). CSE significantly inhibited (38%) arginine uptake in conjunction with a 34% reduction in expression of the arginine transporter, CAT1. In conjunction with these studies, CSE significantly reduced the activity of eNOS and NO production by endothelial cells, while stimulating the production of reactive oxygen species. In conclusion, cigarette smoke adversely affects the endothelial l-arginine NO synthase pathway, resulting in reducing NO production and elevated oxidative stress. In conjunction, exposure to cigarette smoke increases ADMA concentration, the latter being a risk factor for cardiovascular disease.
Language eng
DOI 10.1161/01.HYP.0000231509.27406.42
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Persistent URL http://hdl.handle.net/10536/DRO/DU:30048490

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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