Several recent studies have demonstrated that various forms of hypertension are associated with enhanced reactive oxygen species (ROS) activity. We have recently shown that long-term consumption of a diet similar to that ingested in westernized societies, containing high saturated fat and refined carbohydrate, induces oxidative stress and hypertension in normal rats. We hypothesized that diet modification may reverse diet-induced hypertension via (among other mechanisms) decreased ROS activity and improved nitric oxide (NO) availability. To test this hypothesis, female Fischer rats were placed on either a high-fat (primarily saturated), refined carbohydrate (sucrose) diet (HFS) or low-fat, complex-carbohydrate diet (LFCC) starting at 2 months of age. After 2 years when hypertension was well established, a group of HFS rats was converted to the LFCC diet (HFS/LFCC group) for a period of 2 months. Plasma malondialdehyde, a marker of lipid peroxidation by ROS, was elevated in the HFS group. Hypertension was present in the HFS group at 2 years as was a significant accumulation, in various tissues, of nitrotyrosine, which is the footprint of NO inactivation by ROS. Conversion from the HFS to the LFCC diet for 2 months led to normalization of blood pressure and reduced nitrotyrosine accumulation in the absence of caloric restriction. These results demonstrate that oxidative stress and hypertension induced by long-term consumption of an HFS diet are reversible with implementation of a low-fat, unrefined carbohydrate diet. The effects of the HFS diet and subsequent conversion to the LFCC diet on blood pressure appear to be, in part, mediated by changes in NO availability.