P224 EFFECT OF SODIUM NITRITE ON RENAL DAMAGE FROM 2-KIDNEY, 1-CLIP (2K-1C) HYPERTENSION IN RATS

Renovascular hypertension is characterized by oxidative stress and decreased availability of nitric oxide (NO). Nitrite is a physiologically recycled metabolite that generates NO. Treatment with sodium nitrite has antihypertensive effects due to its antioxidant capacity. However, the renal effects of this treatment are not known in 2K1C hypertension. This study aims to evaluate the effect of treatment with sodium nitrite on kidney damage caused by 2K1C hypertension. Hypertension was induced by cleavage of the left renal artery in Wistar rats. Two weeks after surgery, the animals were treated with two doses (1 mg/kg/day or 15 mg/kg/day) of sodium nitrite or vehicle for 4 weeks, by gavage. Blood pressure (BP) was checked weekly by tail plethysmography. To assess renal function, plasma urea and creatinine were determined. Kidney oxidative stress was evaluated through the activity of catalase (CAT), superoxide dismutase (SOD), levels of reduced glutathione (GSH), lipid peroxidation, and superoxide (O2-) levels. Treatment with 15 mg/kg/day of sodium nitrite reversed the increase in BP in 2K1C rats (p<0.05, 2K1C:170.5±6.542; 2K1C+Nitrite15:162.4±6.712 mmHg), and improved renal function previously impaired by hypertension (urea, p<0.05; 2K1C:76.37±24.53; 2K1C+Nitrite15:47.82±13.86; creatinine, p<0.05; 2K1C:0.540±0.105; 2K1C+Nitrite15:0.3550±0.117). SOD activity decreased in the kidneys of hypertensive animals (p<0.05, Control:0.7176±0.06426; 2K1C:0.636±0.0888; 2K1C+Nitrite1:0.703±0.0866; 2K1C+Nitrite15:0.648±0.173). As for CAT and GSH, there was a decrease in activity in hypertensive animals, with improvement in the group treated with nitrite 15 mg/kg/day (CAT p<0.05, Control:0.651±0.255; 2K1C:0.2772±0.1837; 2K1C+Nitrite15: 0.6654±0.1440 and GSH: p<0.05, Control:44.80±10.59; 2K1C: 29,62±7,253 2K1C+Nitrite15:44.25±10.07). Lipid peroxidation increased by hypertension was reduced with treatment at the highest dosage (p<0.05, Control:0.314±0.158; 2K1C:0.497±0.113; 2K1C+Nitrite15:0.278±0.084). O2- levels were decreased in all groups treated with nitrite (p<0.05, 2K1C:3.844±1.598; 2K1C+Nitrite1:0.9643±0.2063; 2K1C+Nitrite15:0.4431±0.1838). Our results suggest that sodium nitrite treatment improves 2K1C renal damage through its antioxidant activity. Acknowledgments: FAPEMIG# APQ-00946-23, CNPq# 302076/2022-0