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• W2028214912 abstract "Acute inflammation causes endothelial dysfunction, which is partly mediated by oxidant stress and inactivation of nitric oxide. The contribution of depletion of tetrahydrobiopterin (BH 4 ), the cofactor required for nitric oxide generation, is unclear. In this randomized, double-blind, three-way crossover study, forearm blood flow (FBF) responses to ACh and glyceryltrinitrate (GTN) were measured before and 3.5 h after infusion of Escherichia coli endotoxin (LPS, 20 IU/kg iv) in eight healthy men. The effect of intra-arterial BH 4 (500 μg/min), placebo, or vitamin C (24 mg/min) was studied on separate days 3.5 h after LPS infusion. In addition, human umbilical vein endothelial cells were incubated for 24 h with vitamin C and LPS. ACh and GTN caused dose-dependent forearm vasodilation. The FBF response to ACh, which was decreased by 23 ± 17% ( P < 0.05) by LPS infusion, was restored to baseline reactivity by BH 4 and vitamin C. FBF responses to GTN were not affected by BH 4 or vitamin C. LPS increased leukocyte count, high-sensitivity C-reactive protein, IL-6, IL-1β, IFN-γ, monocyte chemoattractant protein-1, pulse rate, and body temperature and decreased platelet count and vitamin C concentration. Vitamin C increased forearm plasma concentration of BH 4 by 32% ( P < 0.02). Incubation with LPS and vitamin C, but not LPS alone, increased intracellular BH 4 concentration in human umbilical vein endothelial cells. Impaired endothelial function during acute inflammation can be restored by BH 4 or vitamin C. Vitamin C may exert some of its salutary effects by increasing BH 4 concentration." @default.
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• W2028214912 date "2005-10-01" @default.
• W2028214912 modified "2023-10-03" @default.
• W2028214912 title "Tetrahydrobiopterin corrects<i>Escherichia coli</i>endotoxin-induced endothelial dysfunction" @default.
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• W2028214912 doi "https://doi.org/10.1152/ajpheart.00057.2005" @default.
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