Fundamental role of axial stress in compensatory adaptations by arteries

• Published in: Journal of biomechanics Vol. 42; no. 1; pp. 1 - 8
• Main Authors: Humphrey, J.D, Eberth, J.F, Dye, W.W, Gleason, R.L
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 05-01-2009; Elsevier Limited
• Subjects: Adaptation, Biological; Animals; Arteries - anatomy & histology; Arteries - metabolism; Arteries - physiology; Biomechanics; Cell culture; Collagen; Elastin; Extracellular Matrix - metabolism; Fibrillin-1; Growth; Hemodynamics; Humans; Hypertension; Muscular dystrophy; Nitric oxide; Physical Medicine and Rehabilitation; Pulmonary arteries; Remodeling; Shear stress; Smooth muscle; Stress, Mechanical; Veins & arteries; Hypertension; Fibrillin-1; Growth; Elastin; Collagen; Remodeling; Muscular dystrophy
• ISSN: 0021-9290; 1873-2380
• DOI: 10.1016/j.jbiomech.2008.11.011

Abstract Arteries exhibit a remarkable ability to adapt to diverse genetic defects and sustained alterations in mechanical loading. For example, changes in blood flow induced wall shear stress tend to control arterial caliber and changes in blood pressure induced circumferential wall stress tend to control wall thickness. We submit, however, that the axial component of wall stress plays a similarly fundamental role in controlling arterial geometry, structure, and function, that is, compensatory adaptations. This observation comes from a review of findings reported in the literature and a comparison of four recent studies from our laboratory that quantified changes in the biaxial mechanical properties of mouse carotid arteries in cases of altered cell-matrix interactions, extracellular matrix composition, blood pressure, or axial extension. There is, therefore, a pressing need to include the fundamental role of axial wall stress in conceptual and theoretical models of arterial growth and remodeling and, consequently, there is a need for increased attention to evolving biaxial mechanical properties in cases of altered genetics and mechanical stimuli.