Cardio-Renal Effects of Short-Term Fructose Treatment in Hypertensive Rats: Focused on NO/ROS Balance

Short-term fructose exposure may perturb the nitric oxide (NO)/reactive oxygen species (ROS) balance before hemodynamic changes development. Male Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) rats received 10 % fructose in drinking water for 3 weeks or remained on tap water. We assessed systolic blood pressure (tail-cuff), plasma lipid levels, tissue conjugated diene concentrations, protein expression of NADPH oxidase, NF-kappaB, and SOD (Western blot), and total NO synthase (NOS) activity ([3H]-L-arginine to [3H]-L-citrulline). Fructose did not change blood pressure in either strain, but increased kidney-to-body-weight ratio in SHR. In WKY, plasma HDL level decreased; in SHR, total cholesterol, VLDL, and triglycerides increased. Conjugated diene concentration increased in the kidney of WKY but not in the heart. Fructose upregulated renal NADPH oxidase and downregulated renal SOD in SHR, with no change in cardiac NADPH oxidase. NF-?B protein expression did not change in either tissue. NOS activity decreased in the heart and kidney of WKY and in the kidney of SHR. We can conclude that even moderate, short-term fructose intake induces strain-dependent dyslipidemia and an early shift of the renal redox milieu toward oxidative stress, accompanied by reduced NOS activity, while leaving blood pressure unchanged. The kidney appears more susceptible than the heart, particularly in the hypertensive background, highlighting the NO/ROS axis as an early target for intervention.