Infusion of angiotensin II (AngII) into hyperlipidemic mice augments atherosclerosis and causes formation of abdominal aortic aneurysms (AAAs). The purpose of this study was to define the contribution of AngII-induced hypertension to these vascular pathologies. Male apolipoprotein E (apoE) and LDL receptor (LDLr) deficient mice were infused with AngII (1,000 ng/kg/min) or norepinephrine (NE; 5.6 mg/kg/day) for 28 days. Infusion of AngII or NE increased mean arterial pressure (MAP; AngII, 133 ± 2.8; NE, 129 ± 13 mmHg) to a similar extent compared to baseline blood pressures (MAP, 107 ± 2 mmHg). Abdominal aortic width increased in both apoE-/- or LDLr-/- mice infused with AngII (apoE-/-: 1.4 ± 0.1; LDLr-/-: 1.6 ± 0.2 mm). In contrast, NE did not change diameters of abdominal aortas (apoE-/-: 0.91 ± 0.03; LDLr-/-: 0.87 ± 0.02 mm). Similarly, atherosclerotic lesions in aortic arches were much greater in mice infused with AngII compared to NE. At a subpressor infusion rate of AngII (500 ng/kg/min), AAAs developed in 50% of apoE-/- mice. Alternatively, administration of hydralazine (250 mg/L) to AngII-infused apoE-/- mice (1,000 ng/kg/min) lowered systolic blood pressure (day 28: AngII, 157 ± 6; AngII/hydralazine, 135 ± 6 mmHg), but did not prevent AAA formation or atherosclerosis. These results demonstrate that infusion of AngII to hyperlipidemic mice induces AAAs and augments atherosclerosis independent of increased blood pressure.