Age-related endothelial dysfunction with respect to nitric oxide, endothelium-derived hyperpolarizing factor and cyclooxygenase products

Title:

Age-related endothelial dysfunction with respect to nitric oxide, endothelium-derived hyperpolarizing factor and cyclooxygenase products

Creator:

Matz, R. L., Schott, C., Stoclet, J. C., and Ramaroson Andriantsitohaina

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a91421a3-92ac-416c-bfe3-e314f9315f57
uuid:a91421a3-92ac-416c-bfe3-e314f9315f57
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, endoteliální dysfunkce, cyklooxygenáza 2, endothelial dysfunction, cyclooxygenase 2, vascular aging, EDHF, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Vascular aging is associated with both structural and functional changes that can take place at the level of the endothelium, vascular smooth muscle cells and the extracellular matrix of blood vessels. With regard to the endothelium, reduced vasodilatation in response to agonists occurs in large conduit arteries as well as in resistance arteries with aging. Reviews concerning the different hypotheses that may account for this endothelial dysfunction have pointed out alterations in the equilibrium between endothelium-derived relaxing and constricting factors. Thus, a decreased vasorelaxation due to nitric oxide and, in some arteries, endothelium-derived hyperpolarizing factor as well as an increased vasoconstriction mediated by cyclooxygenase products such as thromboxane A2 are likely to occur in age-induced impairment of endothelial vasodilatation. Furthermore, enhanced oxidative stress plays a critical role in the deleterious effect of aging on the endothelium by means of nitric oxide breakdown due to reactive oxygen species. The relative contribution of the above phenomenon in age-related endothelial dysfunction is highly dependent on the species and type of vascular bed., R. L. Matz, C. Schott, J. C. Stoclet, R. Andriantsitohaina., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2000 Volume:49 | Number:1

Harvested from:

CDK

Metadata only:

false