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      Reciprocal Expression of Vascular Endothelial Growth Factor and Nitric Oxide Synthase by Coronary Arterial Wall Cells during Chronic Inhibition of Nitric Oxide Synthesis in Rats

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          Chronic inhibition of nitric oxide (NO) synthesis by oral administration of N<sup>G</sup>-nitro- L-arginine methyl ester (L-NAME) causes hypertension and produces arteriosclerosis in rats. Balloon injury induces upregulation of vascular endothelial growth factor (VEGF) in medial smooth muscle cells of the rat arterial wall, and NO secreted by a restored endothelium acts as the negative feedback mechanism that downregulates VEGF expression to basal levels. In this study, we tested the hypothesis that a reciprocal relation between VEGF and NO would be established in a rat model of chronic NO blockade. Male Wister rats received plain drinking water (n = 10) or L-NAME (0.5 mg/ml) in the drinking water (n = 11) for 6 weeks. After 6 weeks, the wall-to-lumen ratios and perivascular fibrosis in the coronary arteries were greater in the L-NAME group than in the control group. NO synthase-positive cells in the intima were abundantly observed in the control group, whereas no such cells were seen in the L-NAME group. In contrast, the number of VEGF-positive smooth muscle cells in the media was greater in the L-NAME group than in the control group. These findings strongly suggest a reciprocal relation between VEGF and NO even in a rat model of chronic NO blockade.

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          Antihypertensive Agents Prevent Nephrosclerosis and Left Ventricular Hypertrophy Induced in Rats by Prolonged Inhibition of Nitric Oxide Synthesis


            Author and article information

            S. Karger AG
            October 2002
            02 September 2002
            : 92
            : 2
            : 472-474
            aDepartment of General Medicine, and bSecond Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan
            63304 Nephron 2002;92:472–474
            © 2002 S. Karger AG, Basel

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