Recovery after dietary vitamin E supplementation of impaired endothelial function in vitamin E-deficient rats.
1. Thoracic aortae, isolated from rats supplemented with dietary vitamin E after vitamin E deficiency, were analysed for changes in vascular reactivity. 2. Following 4 or 12 months of dietary vitamin E deficiency, endothelium-dependent vasodilator responses to acetylcholine were significantly impaired. However, when animals were fed after the first 4 months of vitamin E deprivation with a vitamin E-supplemented diet for 8 months, endothelium-mediated responses were completely restored. 3. In contrast, the endothelium-independent vasodilator or vasoconstrictor responses to sodium nitroprusside and noradrenaline, respectively were not altered either by vitamin E deficiency or supplementation. 4. These data indicate that vitamin E supplementation reversed the impairment of endothelial cell function which occurs during vitamin E deficiency.
Rubino
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A
Department of Anatomy and Developmental Biology, University College London.
Burnstock
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G
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects; D004730:Endothelium, Vascular / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014664:Vasodilation / Q000187:drug effects; D014810:Vitamin E / Q000627:therapeutic use*; D014811:Vitamin E Deficiency / Q000188:drug therapy* / Q000503:physiopathology*
D014810:Vitamin E; D009599:Nitroprusside; D000109:Acetylcholine; D009638:Norepinephrine