Objective: We reported that the endothelial dysfunction that develops with age was associated with a pro-inflammatory phenotype. In this study, we hypothesized that an increased production of pro-inflammatory cyclooxygenase (COX) products occurs before endothelial dysfunction. Methods: Dilations to acetylcholine (ACh) were recorded from pressurised renal arteries isolated from 3- and 6-m/o C57Bl/6 male mice treated or not with the polyphenol catechin (30 mg/kg/day) in the drinking water for 3 months. TXB₂ release, the metabolite of TXA₂, was measured using immuno-enzymatic assays and free radical production was measured using the fluorescent dye CM-H₂DCF-DA. eNOS and COX-1/2 mRNA expression was quantified by qPCR. Results: L-NNA reduced (P<0.05) ACh-induced dilation in vessels isolated from 3- and 6-m/o mice. In the presence of L-NNA, indomethacin normalised (P<0.05) the dilation in vessels from 6-m/o mice only. SQ 29,548 (TP receptor antagonist) and furegrelate (TXA₂ synthase inhibitor), in the presence of L-NNA, also improved (P<0.05) dilation. L-NNA increased TXA₂ release and free radical-associated fluorescence, the latter being prevented by SQ 29,548. In vessels from 6-m/o mice treated with catechin for 3 months, L-NNA-dependent reduction in ACh-mediated dilation was insensitive to indomethacin, while TXA₂ release and free radical-associated fluorescence were prevented. eNOS mRNA expression was significantly increased by catechin treatment. Conclusion: Our results suggest that an augmented production of TXA₂ and the associated change in redox regulation precede the development of the endothelial dysfunction.