Abstract--It is known that the endothelial function is compromised in atherosclerosis and arterial hypertension and that angiotensin is an important factor contributing to both pathophysiologies. The aim of this study was to evaluate the vascular function in a hypercholesterolemia/atherosclerosis model, in the angiotensin II-dependent 2-kidney 1-clip (2K1C) hypertension model and when both conditions coexist. Eight-week-old apolipoprotein E knockout (apoE; n=20) and C57BL/6 (C57; n=20) mice underwent a 2K1C or sham operation and were studied 28 days later. Mean arterial pressure was higher in apoE--2K1C and C57-2K1C (126±3 and 128±3 mm Hg) when compared with the apoE-Sham and C57-Sham (103±2 and 104±2 mm Hg, respectively; P<0.05). The vascular reactivity to norepinephrine (NE; 10^-9 to 2x10^-3 mol/L), acetylcholine (ACh), and sodium nitroprusside (SNP; 10^-10 to 10^-3 mol/L) was evaluated in the mesenteric arteriolar bed through concentration-effect curves. NE caused vascular hyper-reactivity in apoE-Sham, apoE-2K1C, and C57-2K1C (maximal response 146±5, 144±5, and 159±4 mm Hg, respectively) compared with C57-Sham (122±7 mm Hg; P<0.05). The ACh-induced relaxation was smaller (P<0.05) in apoE-2K1C and C57-2K1C (maximal response 53±3% and 46±3%) than in apoE-Sham and C57-Sham mice (78±5% and 73±4%). SNP-induced vascular relaxation showed similar concentration-effect curves in all groups. We conclude that in C57-2K1C mice, the increased reactivity to NE and the decreased endothelium-dependent relaxation contribute to the maintenance of hypertension. The apoE mouse, at early stages of atherosclerosis, shows hyper-reactivity to NE but does not have endothelium dysfunction yet. However, the concurrence of both pathophysiologies does not result in additive effects on the vascular function.