High sodium intake increases vascular superoxide formation and promotes atherosclerosis in apolipoprotein E-deficient mice.

摘要: Hypertension is a major risk factor for atherosclerosis. We tested the hypothesis whether high salt intake aggravates endothelial dysfunction and promotes atherosclerosis in apolipoprotein E-deficient mice (ApoE(-)/(-) mice) their littermate controls (C57Bl/6 mice). The role of increased oxidative stress was also examined. A high-salt diet (NaCl 7%) 12 weeks blood pressure induced cardiac hypertrophy albuminuria more pronouncedly ApoE(-)/(-) compared with C57Bl/6. Endothelium-dependent vascular relaxation response to acetylcholine almost maximally impaired during normal sodium diet. did not further impair NO-mediated relaxation. markedly attenuated endothelium-dependent C57Bl/6 mice. Preincubation superoxide scavenger Tiron normalized function completely both strains indicating central pathogenesis. Aortic production extent atherosclerotic lesions were greater on normal-salt formation promoted Changes dietary influence serum lipids either mouse strains. Our findings suggest detrimental development underscore importance pathogenesis salt-induced damage.