A high-salt diet in rats significantly depressed arteriolar responses to acetylcholine and increased microvascular oxidant levels, which were normalized by oxidant scavengers.
Does a high-salt diet reduce endothelium-dependent dilation via reactive oxygen species generation in normotensive rats?
A high-salt diet impairs endothelium-dependent vasodilation in normotensive rats through increased generation of reactive oxygen species.
In normotensive rats, an increase in dietary salt leads to decreased arteriolar responsiveness to acetylcholine (ACh) because of suppressed local nitric oxide (NO) activity. We evaluated the possibility that generation of reactive oxygen species in the arteriolar wall is responsible for this loss of NO activity. Arteriolar responses to iontophoretically applied ACh were examined in the superfused spinotrapezius muscle of Sprague-Dawley rats fed a low-salt (LS; 0.45%) or high-salt diet (HS; 7%) for 4-5 wk. Responses to ACh were significantly depressed in HS rats but returned to normal in the presence of the oxidant scavengers superoxide dismutase + catalase or 2,2,6, 6-tetamethylpiperidine-N-oxyl (TEMPO) + catalase. Arteriolar responses to the NO donor sodium nitroprusside were similar in HS and LS rats. Arteriolar and venular wall oxidant activity, as determined by reduction of tetranitroblue tetrazolium, was significantly greater in HS rats than in LS rats. Exposure to TEMPO + catalase reduced microvascular oxidant levels to normal in HS rats. These data suggest that a high-salt diet leads to increased generation of reactive oxygen species in striated muscle microvessels, and this increased oxidative state may be responsible for decreased endothelium-dependent responses associated with high salt intake.
Lenda et al. (Sat,) conducted a other in Normotensive. High-salt diet vs. Low-salt diet (0.45%) was evaluated on Arteriolar responses to acetylcholine (ACh) and oxidant activity. A high-salt diet in rats significantly depressed arteriolar responses to acetylcholine and increased microvascular oxidant levels, which were normalized by oxidant scavengers.