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. Hypercholesterolemia impairs systemic vascular  reactivity in response to endothelium-dependent vasodilators, which may be  mediated partly through increased formation of lipid peroxides. However, it is  unclear whether these pathophysiological mechanisms play a role in renal  vascular impairment in experimental hypercholesterolemia. Hence, pigs were  studied after a 3-mo normal ( n  = 7) or high cholesterol (HC)  ( n  = 7) diet, HC diet supplemented daily with antioxidant vitamins E  (100 IU/kg) and C (1000 mg; HC+vitamins,  n  = 5), or normal diet  supplemented with vitamins (N+vitamins,  n  = 5). Renal blood flow was  measured with electron-beam computed tomography before and during infusion of  acetylcholine (Ach). Endothelial function, endothelial and inducible nitric  oxide synthase (NOS), and nitrotyrosine immunoreactivity were studied in renal  arteries  ex vivo . Despite similar cholesterol levels, LDL  oxidizability (lag time, malondialdehyde, and relative electrophoretic  mobility) was increased in pigs that were fed the HC diet but was  significantly decreased in pigs that were fed the HC+vitamins diet. Renal  blood flow response to Ach was blunted in pigs that were fed the HC diet but  was preserved in pigs that were fed the HC+vitamins diet. Maximal relaxation  to Ach was attenuated in pigs that were fed the HC diet compared with those  that were fed the normal diet (51.5 ± 6.4%  versus  97.0  ± 2.9%;  P  &lt; 0.01) but was preserved in pigs that were fed  the HC+vitamins diet (103.1 ± 3.0%;  P  = 0.39) and N+vitamins  diet (87.7 ± 3.0%;  P  = 0.1), as were relaxation responses to  calcium ionophore A23187. Vascular smooth-muscle relaxation to diethylamine  was enhanced in endothelium-denuded HC vessel but was restored in pigs that  were on the HC+vitamins regimen. In HC, immuno-reactivity of endothelial NOS  was decreased, that of inducible NOS was increased, and both were preserved in  pigs that were fed the HC+vitamins and N+vitamins diets, whereas nitrotyrosine  was not detected. The present study demonstrates that antioxidant intervention  in experimental HC reduces LDL oxidizability and preserves renal vascular  responses to endothelium-dependent vasodilators. Therefore, this beneficial  effect potentially can protect the kidney from hypercholesterolemia-induced  damage.

Renal Vascular Function in Hypercholesterolemia Is Preserved by Chronic Antioxidant Supplementation