Why the study?
Does a high-salt diet impair NO release and increase superoxide production in the aorta of Sprague-Dawley rats?
Does a high-salt diet impair NO release and increase superoxide production in the aorta of Sprague-Dawley rats?
A high-salt diet rapidly impairs endothelium-dependent relaxation in rat aortas by reducing nitric oxide levels and increasing superoxide production.
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High-salt diet may impair endothelial NO via superoxide in rats; leaves open relevance to human hypertension.
Sprague-Dawley rats were fed either a high-salt (HS) diet (4.0% NaCl) or a low-salt (LS) diet (0.4% NaCl) for 3 days. Nitric oxide (NO) and superoxide production were assessed in the thoracic aorta by evaluating the fluorescence signal intensity from 4,5-diaminofluorescein (DAF-2DA) and dihydroethidine, respectively. Methacholine caused increased NO release in the aortas from rats on a LS but not HS diet. The SOD mimetic tempol restored methacholine-induced NO release in aortas from rats on a HS diet. Methacholine also caused superoxide production in the aortas of rats on a HS diet but not in the aortas of rats on a LS diet. Tempol and N(G)-monomethyl-l-arginine eliminated methacholine-induced superoxide production in the aortas of rats on a HS diet. Aortic rings from rats on the HS diet showed impaired methacholine-induced relaxation, which was improved by tempol. Tempol alone caused a NO-dependent relaxation of norepinephrine-precontracted aortas that was significantly greater in the aortas of rats on the HS diet than in vessels from rats on the LS diet. These data suggest that a HS diet impairs endothelium-dependent relaxation via reduced NO levels and increased superoxide production.
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Zhu et al. (2004) studied this question.
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