We have reported that pharmacological doses of oral nitrite increase circulating nitric oxide (NO) and exert hypotensive effects in L-NAME-induced hypertensive rats. In this study, we examined the effect of a chronic dietary dose of nitrite on the hypertension and renal damage induced by chronic L-NAME administration in rats. The animals were administered tap water containing L-NAME (1g/L) or L-NAME+nitrite (Low dose:0.1mg/L, Medium dose:1mg/L, High dose:10mg/L) for eight weeks. We evaluated the blood NO levels as hemoglobin-NO adducts (iron-nitrosyl-hemoglobin) using an electron paramagnetic resonance (EPR)method. Chronic administration of L-NAME for 8 weeks induced hypertension and renal injury and reduced the blood iron-nitrosyl-hemoglobin level (control;38.8±8.9 vs L-NAME; 6.0±3.1 arbitrary units). Co-administration of a low dose of nitrite with L-NAME did not change the reduced iron-nitrosyl-hemoglobin signal and did not improve the L-NAME-induced renal injury. The blood iron-nitrosyl-hemoglobin signals of the medium dose and high dose of nitrite were significantly higher than that of L-NAME alone. Chronic administration of a medium dose of nitrite attenuated L-NAME-induced renal histrogical changes and proteinuria. A high dose of nitrite also attenuated L-NAME-induced renal injury. These findings suggest that dietary doses of nitrite that protect the kidney are associated with significant increase in iron-nitrosyl-hemoglobin levels. We conclude dietary nitrite-derived NO generation may serve as a backup system when the NOS/L-arginine-dependent NO generation system is compromised.