Background: The sympathetic autonomic nervous system plays important role in the control of the vascular tone. Altered vasoconstriction to α1-adrenoceptor (α1AR) activation occurs in hypertension. Aim: To evaluate the role of superoxide anion (O2−), hydrogen peroxide (H2O2) and COX-1 and COX-2 on the contraction induced by α1AR agonist phenylephrine (PE) in aortas isolated from normotensive (2K) and 2K-1C. Methods: Concentration-effect curves were performed for PE in 2K and 2K-1C intact (E+) or denuded (E−) aorta, in the absence or presence of O2− scavenger Tiron or Catalase, or selective inhibitors of COX-1 (SC-560;10 μM) or COX-2 (SC-236;10 μM). Results: PE induced similar ME and pD2 in E− 2K (2.5±0.2 g; 7.93±0.10; n=8) and 2K-1C (2.6±0.2 g; 7.89±0.08; n=9). Potency was lower in (E+) 2K and 2K-1C than in E−, while ME was reduced only in 2K-1C (2K, ME:2.2±0.1 g; pD2:7.44±0.03; n=5 and 2K-1C, ME:1.2±0.2 g; pD2:7.54±0.06; n=7; p<0.001). In E+, the efficacy of PE was higher in 2K than in 2K-1C. O2− scavenger Tiron 0.1 mM, reduced contraction to PE only in 2K E− (ME:2.4±0.2 g; pD2:7.60±0.06; n=8). Catalase reduced the contraction to PE only in 2K-1C E− (ME:1.9±0.2 g; pD2:7.64±0.03; n=3; p<0.001) that was increased in 2K-1C E+ (ME:1.75±0.2 g; pD2:7.67±0.07; n=3; p<0.001). Incubation of 2K (E+) or (E-) with SC-560 reduced only the potency of PE. SC-560 reduced potency and efficacy of PE only in E− from 2K-1C. SC-236, reduced the potency and efficacy of PE in E+ or E− from 2K. SC-236 was more potent in 2K than 2K-1C, and the contraction to PE was almost abolished in 2K E+, but not in 2K-1C. Conclusion: O2− plays important role on the contraction induced by PE in 2K while H2O2 has important role in 2K-1C aorta. The contribution of COX products to contraction to PE has a dual effect. COX-1 is important in 2K-1C whereas COX-2 is important in 2K.