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Updated: Jul 11, 2026
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Evaluation of aortic remodeling in apolipoprotein E-deficient mice and renovascular hypertensive mice
Breno V Nogueira1, Veronica A Peotta, Silvana S Meyrelles
1Laboratory of Transgenes and Cardiovascular Control, Physiological Sciences Graduate Program, Health Sciences Center, Federal University of Espirito Santo, Vitoria, ES, Brazil.
Background:
The apolipoprotein E-deficient mouse (ApoE) spontaneously develops hypercholesterolemia and atherosclerotic lesions in large arteries. It is also known that angiotensin II-induced hypertension accelerates the development of atherosclerosis in ApoE mice. The objective of this study was to evaluate the aortic remodeling process in ApoE mice during the early phase of atherosclerosis in two-kidney one-clip hypertensive (2K1C) mice and in mice with the coexistence of atherosclerosis and arterial hypertension.
Methods:
Renovascular hypertension was induced in 8- to 9-week-old C57BL/6 (C57) and ApoE and compared to sham animals 28 days later. C57-2K1C and ApoE-2K1C mice showed hypertension, tachycardia, and cardiac hypertrophy of similar magnitude.
Results:
ApoE and ApoE-2K1C mice showed high levels of plasma cholesterol (4.8- and 3.6-fold) and aorta lipid deposition (85- and 101-fold) compared to C57 mice. The aorta lumen area was increased in C57-2K1C and ApoE-2K1C mice (0.57 +/- 0.04 and 0.55 +/- 0.02 mm(2)) compared to C57 mice (0.50 +/- 0.02 mm(2), p <0.05). The aorta wall area was increased by 20% in C57-2K1C and by 12% in ApoE-2K1C mice compared to C57 and ApoE.
Conclusions:
The main finding of this study was the absence of aorta remodeling in ApoE mice at the early stage of atherosclerosis and an outward remodeling of similar magnitude in C57-2K1C and ApoE-2K1C mice.
