Elastin and collagen are the main structural components in the extracellular matrix (ECM) that contribute to the anisotropic and hyperelastic passive mechanical behavior of elastic arteries. It is commonly accepted that the elastin fibers support most of the load at the onset of stretching while collagen fiber recruitment and the transition to collagen bearing the load occurs at higher pressures [1]. Various diseases lead to changes in the ECM, for example in aortic aneurysm there is reduced elastin, excess aged collagen, and fragmentation of the elastic lamellae [2]. Likewise hypertension has been shown to increase arterial collagen and wall thickness with increased stiffness [3]. Improving our knowledge of how the ECM structure affects the mechanical behavior of arteries can provide insights to disease progression and better treatment methods.

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