Objective To investigate the possible mechanisms of aging-associated vascular dysfunction by peroxynitrite (ONOO-) decomposition catalyst FeTMPyP. Methods Male Sprague-Dawlew (SD) rats were randomly divided into three groups: adult group (3-4-month-old, n=8), aging group (18-20-month-old, n=8), and FeTMPyP treatment aging group (n=6). The thoracic aorta was isolated for measurement of vascular diastolic function. Immunohistochemistry and Western-blot were performed to determine the expression of 3-nitrotyrosine (3-NT, a marker of ONOO- formation) in thoracic aortic arteries. Results (1) Comparing with adult group, the maximal vasodilation in aging rats induced by acetylcholine (ACh, an endothelium-dependent vasodilator, 10-9 to 10-5 mol/L) was significantly decreased from (69.52% ± 5.51%) to (29.74% ± 8.28%) (P＜0.001); the maximal vasodilation induced by sodium nitroprusside (SNP, an endothelium-independent vasodilator, 10-9 to 10-5 mol/L) was also decreased from (99.26% ± 1.33%) to (92.01% ± 3.19%) (P＜0.001). (2) The expression of 3-NT in aging vascular tissues was increased (P＜0.05) compared with adult group. (3) In aging rats treated with FeTMPyP, the expression of 3-NT was decreased (P＜0.01). Moreover, FeTMPyP significantly improved vascular endothelium- dependent and endothelium-independent vasodilations in aging rats. After inhibiting the generation of ONOO-, ACh-induced maximal vasorelaxation was markedly increased [(65.96%±11.36%) vs (29.74%±8.28%), P＜0.001] and SNP-induced maximal vasodilation was also increased [(98.15%±2.79%) vs (92.01%±3.19%), P＜0.001]. Conclusion FeTMPyP can improve vasodilation dysfunction in aging rats, suggesting that ONOO- may play an important role in aging-related vascular dysfunction.