Active Versus Passive Contributions to Age-Related Arterial Stiffness
Arterial stiffening is an important problem in aging, contributing to hypertension, cardiac remodeling, and other problems. The contributing factors are described in the paper noted here, with changes in the behavior of cells controlling constriction and dilation of vessels on the one hand, versus changes in the extracellular matrix that reduce tissue elasticity on the other hand. There remains comparatively little research and development aimed at repair of the aged extracellular matrix, but it is nonetheless important.
Arterial stiffness, a recognized marker of vascular health, reflects the elasticity and compliance of arteries. Central arterial stiffness, as measured by pulse wave velocity, is a predictor of cardiovascular events and mortality independent of traditional risk factors. Arterial stiffness is multifaceted, comprised of both active and passive stiffness. Aging is associated with increased arterial stiffness, caused by changes in active and passive arterial stiffness.
The active contribution to arterial stiffness, otherwise known as vascular tone, is regulated by vascular smooth muscle cells (VSMCs) and endothelial cells (ECs). ECs, lining the inner surface of blood vessels, contribute towards vascular tone by releasing bioactive molecules that modulate vasoconstriction and vasodilation of VSMCs. Nitric oxide (NO), a key endothelium-derived vasodilator, is crucial for maintaining proper vessel function. EC dysfunction leads to impaired NO production, contributing towards augmented vasoconstriction, oxidative stress, and ultimately, cardiovascular diseases.
Passive stiffness encompasses extracellular matrix (ECM) structural proteins. Collagen and elastin are important structural proteins in ECM, contributing to mechanical properties of blood vessels. Collagen provides tensile strength, while elastin confers elasticity. The balanced interaction between collagen and elastin is vital for maintaining arterial integrity, allowing blood vessels to withstand mechanical stress. Arterial tissues from different anatomical regions on the aorta exhibit distinct mechanical properties and endothelial responses due to variations in structure, hemodynamics, and local microenvironments.