The aim of the present study was to evaluate the effect of overstimulation of the -adrenoceptors on vascular inflammatory mediators. Wistar rats were treated with the -adrenoceptor agonist isoproterenol (0.3 mg kg^-1 day^-1, sc) or vehicle (control) for 7 days. At the end of treatment, right carotid artery was catheterized for arterial and left ventricle (LV) haemodynamic evaluation. Isoproterenol-treatment increased LV weight but did not change haemodynamic parameters. Aortic mRNA and protein expression were quantified by real time RT-PCR and Western-blot, respectively. Isoproterenol enhanced aortic mRNA and protein expression of IL-1 (124% and 125%), IL-6 (231% and 40%) compared to controls, but did not change TNF- expression. The ratio nuclear/cytoplasmatic protein expression of NF-B p65 subunit was increased by isoproterenol-treatment (51%), beside it reduced cytoplasmatic expression of IB-(52%) in aortas. Electrophoretic mobility shift assay was performed in aorta and increased NF-B DNA binding (31%) were observed in isoproterenol-treated rats compared to controls (p<0.05). Isoproterenol-treatment increased phenylephrine-induced contraction in aortic rigs (p<0.05), which was significantly reduced by superoxide dismutase (SOD, 150 U mL^-1) and sodium salicylate (NaSal, 5mM). Co-treatment with thalidomide (150 mg kg^-1 day^-1, 7 days) also reduced hyperreactivity to phenylephrine induced by isoproterenol. In conclusion, overstimulation of -adrenoceptors increased proinflammatory cytokines and up-regulates NF-B in rat aorta. Moreover, local oxidative stress and proinflammatory state seems to play a key role in the altered vascular reactivity of rat aorta induced by chronic -adrenergic stimulation.