Vascular stiffness: measurements, mechanisms and implications

• Published in: Current vascular pharmacology Vol. 2; no. 4; p. 379
• Main Authors: Wang, Yi-Xin, Fitch, Richard M
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.10.2004
• Subjects: Angiotensin II - physiology; Animals; Anti-Inflammatory Agents - pharmacology; Arteries - physiopathology; Arteriosclerosis - etiology; Arteriosclerosis - physiopathology; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Estrogens - pharmacology; Humans; Inflammation - complications; Nitric Oxide - metabolism; Nitric Oxide - physiology; Vascular Resistance - drug effects; Vascular Resistance - physiology
• ISSN: 1570-1611
• DOI: 10.2174/1570161043385448

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.