Advancing age is the major risk factor for the development of CVD (cardiovascular diseases). This is attributable, in part, to the development of vascular endothelial dysfunction, as indicated by reduced peripheral artery EDD (endothelium-dependent dilation) in response to chemical [typically ACh (acetylcholine)] or mechanical (intravascular shear) stimuli. Reduced bioavailability of the endothelium-synthesized dilating molecule NO (nitric oxide) as a result of oxidative stress is the key mechanism mediating reduced EDD with aging. Vascular oxidative stress increases with age as a consequence of greater production of reactive oxygen species (e.g. superoxide) without a compensatory increase in antioxidant defences. Sources of increased superoxide production include up-regulation of the oxidant enzyme NADPH oxidase, uncoupling of the normally NO-producing enzyme, eNOS (endothelial NO synthase) (due to reduced availability of the cofactor tetrahydrobiopterin) and increased mitochondrial synthesis during oxidative phosphorylation. Increased bioactivity of the potent endothelial-derived constricting factor ET-1 (endothelin-1), reduced endothelial production of/responsiveness to dilatory prostaglandins, the development of vascular inflammation, formation of AGEs (advanced glycation end-products), an increased rate of endothelial apoptosis and reduced expression of oestrogen receptor α (in postmenopausal females) also probably contribute to impaired EDD with aging. Several lifestyle and biological factors modulate vascular endothelial function with aging, including regular aerobic exercise, dietary factors (e.g. processed compared with non-processed foods), body weight/fatness, vitamin D status, menopause/oestrogen deficiency and a number of conventional and non-conventional risk factors for CVD. Given the number of older adults now and in the future, more information is needed on effective strategies for the prevention and treatment of vascular endothelial aging.
Skip Nav Destination
Close
Article navigation
Review Article|
January 18 2011
Aging and vascular endothelial function in humans
Douglas R. Seals
;
1Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, U.S.A.
Correspondence: Professor Douglas R. Seals (email seals@colorado.edu).
Search for other works by this author on:
Kristen L. Jablonski
;
Kristen L. Jablonski
1Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, U.S.A.
Search for other works by this author on:
Anthony J. Donato
Anthony J. Donato
1Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, U.S.A.
Search for other works by this author on:
Clin Sci (Lond) (2011) 120 (9): 357–375.
Article history
Received:
September 23 2010
Revision Received:
November 10 2010
Accepted:
November 11 2010
Citation
Douglas R. Seals, Kristen L. Jablonski, Anthony J. Donato; Aging and vascular endothelial function in humans. Clin Sci (Lond) 1 May 2011; 120 (9): 357–375. doi: https://doi.org/10.1042/CS20100476
Download citation file:
Close
Sign in
Don't already have an account? Register
Sign in to your personal account
You could not be signed in. Please check your email address / username and password and try again.
Biochemical Society Member Sign in
Sign InSign in via your Institution
Sign in via your InstitutionGet Access To This Article
Cited By
Related Articles
Local endothelial DNA repair deficiency causes aging-resembling endothelial-specific dysfunction
Clin Sci (Lond) (April,2020)
Sex-specific effects of habitual aerobic exercise on brachial artery flow-mediated dilation in middle-aged and older adults
Clin Sci (Lond) (September,2010)
Prevention of age-related endothelial dysfunction by habitual aerobic exercise in healthy humans: possible role of nuclear factor κB
Clin Sci (Lond) (July,2014)
Skeletal muscles of aged male mice fail to adapt following contractile activity
Biochem Soc Trans (April,2003)