期刊
AMERICAN JOURNAL OF HYPERTENSION
卷 17, 期 1, 页码 31-36出版社
OXFORD UNIV PRESS
DOI: 10.1016/j.amjhyper.2003.08.003
关键词
Dahl rats; glutathione; oxidative stress; endothelium-derived relaxing factors
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR011104] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [S06GM008248] Funding Source: NIH RePORTER
- NCRR NIH HHS [P20RR11104-06] Funding Source: Medline
- NIGMS NIH HHS [S06GM08248-12] Funding Source: Medline
Background: Impairment of endothelial function during hypertension is associated with increased production of superoxide radicals and reduced antioxidants. We investigated the involvement of oxidative stress in Dahl salt-sensitive (SS) and salt-resistant (SR) rats. Methods: For a 2-week period, male rats were fed either high salt (HS; 8% sodium chloride) or low salt (LS; 0.3% sodium chloride) diets. Before and weekly on the diets, mean arterial pressure (MAP) and heart rate were measured by tail-cuff plethysmography. At the end of the experiment, plasma and tissue samples were collected for analysis of nitric oxide, prostacyclin, glutathione, and isoprostane. Results: The MAP was increased in SS rats on HS diet, but not in those on a LS diet or in SR rats on either diet. Plasma levels of nitric oxide were reduced in SS rats on HS diet. Plasma prostacyclin levels in SS rats on either diet were lower than SR on LS diet. Increased dietary salt reduced plasma prostacyclin levels in SR, but not in SS rats. Plasma total 8-isoprostane was elevated in both SS and SR rats on HS diet compared with either strain on LS diet. Plasma levels of total glutathione were reduced in SS compared with SR rats, regardless of the level of dietary salt intake. The whole blood ratio of reduced-to-oxidized glutathione (GSH/GSSG) as well as the kidney total glutathione were lower in SS rats on HS diet. Aortic superoxide production in both strains on HS diet was increased compared with the animals on LS diet. Conclusions: These data suggest that HS diet may indirectly induce endothelial dysfunction through intermediate mechanisms that are associated with oxidative stress. (C) 2004 American Journal of Hypertension, Ltd.
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