The apolipoprotein E-deficient (apoE^-/-) mouse model has advanced our understanding of cardiovascular disease mechanisms and experimental therapeutics. This spontaneous model recapitulates aspects of human atherosclerosis, and allows for the development of dissecting abdominal aortic aneurysms (AAAs) when combined with angiotensin II. We characterized apoE^-/- rats and hypothesized that, similar to mice, they would develop dissecting AAAs. We created rats with a 16-bp deletion of the apoE gene using transcription activator-like effector nucleases. We imaged the suprarenal aorta for 28 days after implantation of miniosmotic pumps that infuse angiotensin II (AngII, 200 ng/kg/min). Blood pressure (BP), serum lipids and lipoproteins, and histology were also analyzed. These rats did not develop pathological aortic dissection, but we did observe a decrease in circumferential cyclic strain, a rise in BP, and microstructural changes in the aortic medial layer. We also measured increased serum lipids with and without administration of a high-fat diet, but did not detect atherosclerotic plaques. Chronic infusion of AngII did not lead to the formation of dissecting AAAs or atherosclerosis in the rats used in this study. While reduced amounts of atherosclerosis may explain this resistance to dissecting aneurysms, further investigation is needed to fully characterize species-specific differences.