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Excessive Adventitial Remodeling Leads to Early Aortic Maladaptation in Angiotensin-Induced Hypertension. Hypertension 2016 May;67(5):890-896

Date

03/24/2016

Pubmed ID

27001298

Pubmed Central ID

PMC4833633

DOI

10.1161/HYPERTENSIONAHA.115.06262

Scopus ID

2-s2.0-84961392963   62 Citations

Abstract

The primary function of central arteries is to store elastic energy during systole and to use it to sustain blood flow during diastole. Arterial stiffening compromises this normal mechanical function and adversely affects end organs, such as the brain, heart, and kidneys. Using an angiotensin II infusion model of hypertension in wild-type mice, we show that the thoracic aorta exhibits a dramatic loss of energy storage within 2 weeks that persists for at least 4 weeks. This diminished mechanical functionality results from increased structural stiffening as a result of an excessive accumulation of adventitial collagen, not a change in the intrinsic stiffness of the wall. A detailed analysis of the transmural biaxial wall stress suggests that the exuberant production of collagen results more from an inflammatory response than from a mechano-adaptation, hence reinforcing the need to control inflammation, not just blood pressure. Although most clinical assessments of arterial stiffening focus on intimal-medial thickening, these results suggest a need to measure and control the highly active and important adventitia.

Author List

Bersi MR, Bellini C, Wu J, Montaniel KRC, Harrison DG, Humphrey JD



MESH terms used to index this publication - Major topics in bold

Adventitia
Analysis of Variance
Angiotensin II
Animals
Aorta
Blood Pressure
Disease Models, Animal
Hypertension
Male
Mice
Mice, Inbred C57BL
Random Allocation
Stress, Physiological
Vascular Remodeling
Vascular Stiffness