Vitamins C and E improve endothelial dysfunction in intrauterine-undernourished rats by decreasing vascular superoxide anion concentration.

J Cardiovasc Pharmacol

Laboratory of Hypertension, Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, 05508-900 Av Prof Lineu Prestes, 1524-São Paulo, Brazil.

Published: August 2003

Epidemiological studies suggest that intrauterine undernutrition plays an important role in the development of arterial hypertension in adulthood. Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have antioxidant properties that could improve redox-sensitive vascular changes associated with hypertension. The authors determined whether vitamins C and E treatments ameliorate the hypertension and vascular function in male rats submitted to intrauterine undernutrition. Pregnant Wistar rats were fed either normal or 50% of the normal intake diets during the whole gestational period. At 14 weeks of age, male offspring of nutritionally restricted dams were divided into 3 subgroups: vehicle-treated (vehicle for 15 days, by gastric gavage, n = 9), vitamin C-treated (ascorbic acid, 150 mg/Kg/d for 15 days, by gastric gavage, n = 15) and vitamin E-treated (alpha-tocopherol, 350 mg/kg per day for 15 days, by gastric gavage, n = 15). Systolic blood pressure was determined before and after antioxidant treatments by the tail-cuff method. At 16 weeks of age, the rats were used for the study of microvascular reactivity and intravital fluorescence microscopy. Intrauterine undernutrition induced hypertension, and vitamins C or E treatments reduced the blood pressure levels. The decreased acetylcholine and bradykinin-induced vasodilation was restored in the vitamin-treated rats. These effects were associated with decreased vascular superoxide anion concentration. The results show that vitamins C and E reduce oxidative stress and high blood pressure levels, and improve vascular function in intrauterine-undernourished rats.

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http://dx.doi.org/10.1097/00005344-200308000-00009DOI Listing

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