This study analyzes the role of angiotensin II (Ang II), via AT 1 receptors, in the involvement of cyclooxygenase (COX)-2-derived prostanoids in phenylephrine responses in normotensive rats (Wistar Kyoto; WKY) and spontaneously hypertensive rats (SHR). Aorta from rats untreated or treated for 12 weeks with losartan (15 mg/kg ⅐ day) or hydralazine plus hydrochlorothiazide (44 and 9.4 mg/kg ⅐ day, respectively) and vascular smooth muscle cells (VSMC) from SHR were used. Vascular reactivity was analyzed by isometric recording; COX-2 expression by Western blot and reverse transcription-polymerase chain reaction; prostaglandin (PG)I 2 , PGF 2␣ , 8-isoprostane, and total antioxidant status (TAS) by commercial kits; superoxide anion (O 2 . ) by lucigenin chemiluminescence; and plasmatic malondi- . production, and MDA levels were higher in SHR, but TAS was similar in both strains.Losartan, but not hydralazine-hydrochlorothiazide treatment, reduced COX-2 expression and the effect of NS-398 on phenylephrine responses in SHR. Losartan also increased TAS and reduced PGF 2␣ , PGI 2 , 8-isoprostane, and O 2 . production and MDA levels in SHR. Ang II (0.1 M) induced COX-2 expression in VSMC from SHR that was reduced by 30 M apocynin and 100 M allopurinol, NADPH oxidase, and xanthine oxidase inhibitors, respectively. In conclusion, AT 1 receptor activation by Ang II could be involved in the increased participation of COX-2-derived contractile prostanoids in vasoconstriction to phenylephrine with hypertension, probably through COX-2 expression regulation. The increased oxidative stress seems to be one of the mechanisms involved.