Abstract
Aging is the dominant process altering vascular stiffness. Risk factors for cardiovascular disease, such as smoking, hypertension and diabetes mellitus, mediate their effects by altering the structure, properties, and function of the vascular wall and endothelial components. Increased vascular stiffness exerts greater afterload stress on the heart. The ability to detect and monitor changes in the physical properties of arteries holds potential to intervene for prevention or attenuation of disease progression. Pulse wave velocity has been used as an index for vascular stiffness and as a surrogate marker for atherosclerosis in laboratory animal models and in the clinic. Mouse models have been used extensively in vascular research. We and others have developed invasive and noninvasive methods to measure pulse wave velocity in rodents, such as rats and mice. Here we review the evidence that the development of atherosclerosis contributes greatly to vascular stiffening; that endothelial nitric oxide plays an important role in modulating vascular stiffness; that angiotensin II injures the vessel and increases vascular stiffness; and that treatment with estrogen attenuates vascular inflammation and reduces vascular stiffness. In addition, we also discuss the influence of hemodynamic, metabolic, inflammatory stimuli in impairing arterial wall integrity as well as potential mechanisms modulating vascular stiffness.
Keywords: vascular stiffness, pulse wave velocity, atherosclerosis, nitric oxide, angiotensin II, estrogen
Current Vascular Pharmacology
Title: Vascular Stiffness: Measurements, Mechanisms and Implications
Volume: 2 Issue: 4
Author(s): Yi-Xin Wang and Richard M. Fitch
Affiliation:
Keywords: vascular stiffness, pulse wave velocity, atherosclerosis, nitric oxide, angiotensin II, estrogen
Abstract: Aging is the dominant process altering vascular stiffness. Risk factors for cardiovascular disease, such as smoking, hypertension and diabetes mellitus, mediate their effects by altering the structure, properties, and function of the vascular wall and endothelial components. Increased vascular stiffness exerts greater afterload stress on the heart. The ability to detect and monitor changes in the physical properties of arteries holds potential to intervene for prevention or attenuation of disease progression. Pulse wave velocity has been used as an index for vascular stiffness and as a surrogate marker for atherosclerosis in laboratory animal models and in the clinic. Mouse models have been used extensively in vascular research. We and others have developed invasive and noninvasive methods to measure pulse wave velocity in rodents, such as rats and mice. Here we review the evidence that the development of atherosclerosis contributes greatly to vascular stiffening; that endothelial nitric oxide plays an important role in modulating vascular stiffness; that angiotensin II injures the vessel and increases vascular stiffness; and that treatment with estrogen attenuates vascular inflammation and reduces vascular stiffness. In addition, we also discuss the influence of hemodynamic, metabolic, inflammatory stimuli in impairing arterial wall integrity as well as potential mechanisms modulating vascular stiffness.
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Cite this article as:
Wang Yi-Xin and Fitch M. Richard, Vascular Stiffness: Measurements, Mechanisms and Implications, Current Vascular Pharmacology 2004; 2 (4) . https://dx.doi.org/10.2174/1570161043385448
DOI https://dx.doi.org/10.2174/1570161043385448 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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