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Research Paper

Angiotensin II Infusion Does Not Cause Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Rats

Phillips E.H.a · Chang M.S.a · Gorman S.a · Qureshi H.J.a · Ejendal K.F.K.a · Kinzer-Ursem T.L.a · Blaize A.N.a, b · Goergen C.J.a, c

Author affiliations

aWeldon School of Biomedical Engineering, bDepartment of Health and Kinesiology, and cPurdue Center for Cancer Research, Purdue University, West Lafayette, IN, USA

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J Vasc Res 2018;55:1-12

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: March 04, 2017
Accepted: October 07, 2017
Published online: November 23, 2017
Issue release date: Published online first

Number of Print Pages: 12
Number of Figures: 6
Number of Tables: 1

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: https://www.karger.com/JVR

Abstract

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.

© 2017 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: March 04, 2017
Accepted: October 07, 2017
Published online: November 23, 2017
Issue release date: Published online first

Number of Print Pages: 12
Number of Figures: 6
Number of Tables: 1

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: https://www.karger.com/JVR


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