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Disparate changes in the mechanical properties of murine carotid arteries and aorta in response to chronic infusion of angiotensin-II

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Abstract

Chronic infusion of angiotensin-II (Ang-II) has proved useful for generating dissecting aortic aneurysms in atheroprone mice. These lesions preferentially form in the suprarenal abdominal aorta and sometimes in the ascending aorta, but reasons for such localization remain unknown. This study focused on why these lesions do not form in other large (central) arteries. Toward this end, we quantified and compared the geometry, composition, and biaxial material behavior (using a nonlinear constitutive relation) of common carotid arteries from three groups of mice: non-treated controls as well as mice receiving a subcutaneous infusion of Ang-II for 28 days that either did or did not lead to the development of a dissecting aortic aneurysm. Consistent with the mild hypertension induced by the Ang-II, the carotid wall thickened as expected and remodeled modestly. There was no evidence, however, of a marked loss of elastic fibers or smooth muscle cells, each of which appear to be initiating events for the development of aneurysms, and there was no evidence of intramural discontinuities that might give rise to dissections.

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Notes

  1. High fat diets are often used to accelerate the development of atherosclerosis in ApoE−/− mice, but our goal was to determine changes in wall properties independent of atherosclerosis.

  2. Our results for the suprarenal aorta are found elsewhere [10, 24].

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Acknowledgments

This work was supported, in part, by a grant from the National Institute of Health (HL105297) as well as generous contributions to Texas A&M University by Carolyn S. and Tommie E. Lohman. This paper is dedicated to Professor K.R. Rajagopal, on the occasion of his 60th birthday.

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Correspondence to J. D. Humphrey.

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M. R. Bersi and M. J. Collins contributed equally.

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Bersi, M.R., Collins, M.J., Wilson, E. et al. Disparate changes in the mechanical properties of murine carotid arteries and aorta in response to chronic infusion of angiotensin-II. Int J Adv Eng Sci Appl Math 4, 228–240 (2012). https://doi.org/10.1007/s12572-012-0052-4

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