INVOLVEMENT OF NITRIC OXIDE AND REACTIVE OXYGEN SPECIES IN CARDIOVASCULAR DISFUNCTION OF RATS WITH OBESITY INDUCED BY MONOSODIUM GLUTAMATE

Abstract

We investigate the involvement of nitric oxide (NO) and reactive oxygen species (ROS) on autonomic, cardiovascular parameters and endothelial cells isolated from aorta in monosodium glutamate (MSG) obese rats. Obesity was induced by administration of 4 mg/g body weight of MSG or equimolar saline (CTR) in newborn rats. At 60th day, treatment was started with L‐NAME (20 mg/kg) or 0.9% saline. At 90th day, artery catheterization was done and after 24 hours, mean arterial pressure (MAP) and heart rate (HR) were recorded. Plasma was collected to assess lipid peroxidation. Endothelial cells were evaluated by flow cytometry and fluorescence intensity (FI) emitted by NO‐sensitive dye (DAF‐2DA) and sensitive to ROS (DHE). MSG is hypertensive compared to CTR. Treatment with L‐NAME increased MAP only in CTR. The MSG induced increase in LF band and decrease in HF band of heart rate variability. The treatment with L‐NAME increased LF band of SAP in CTR without changes in MSG. Lipid peroxidation was higher in MSG and attenuated after L‐NAME. Basal FI to DAF was higher in CTR than MSG. Both groups, acetylcholine increased IF for DAF from basal. However, those values were lower in MSG than CTR. IF baseline to DHE was higher in MSG than CTR. Acetylcholine increased FI to DHE, but this effect was lower in CTR than MSG. We suggest that lower NO bioavailability and increased production of ROS may contribute to elevated blood pressure in MSG animals.