The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Vascular endothelial dysfunction with aging: endothelin-1 and endothelial nitric oxide synthase
Open accessAbstract
To determine whether impaired endothelium-dependent dilation (EDD) in older adults is associated with changes in the expression of major vasoconstrictor or vasodilator proteins in the vascular endothelium, endothelial cells (EC) were obtained from the brachial artery and peripheral veins of 56 healthy men, aged 18–78 yr. Brachial artery EC endothelin-1 (ET-1) [0.99 ± 0.10 vs. 0.57 ± 0.10 ET-1/human umbilical vein EC (HUVEC) intensity, P = 0.01] and serine 1177 phosphorylated endothelial nitric oxide synthase (PeNOS) (0.77 ± 0.09 vs. 0.44 ± 0.07 PeNOS/HUVEC intensity, P < 0.05) (quantitative immunofluorescence) were greater, and EDD (peak forearm blood flow to intrabrachial acetylcholine) was lower (10.2 ± 0.9 vs. 14.7 ± 1.7 ml·100 ml−1·min−1, P < 0.05) in older ( n = 18, 62 ± 1 yr) vs. young ( n = 15, 21 ± 1 yr) healthy men. EDD was inversely related to expression of ET-1 ( r = −0.39, P < 0.05). Brachial artery EC eNOS expression did not differ significantly with age, but tended to be greater in the older men (young: 0.23 ± 0.03 vs. older: 0.33 ± 0.07 eNOS/HUVEC intensity, P = 0.08). In the sample with venous EC collections, EDD (brachial artery flow-mediated dilation) was lower (3.50 ± 0.44 vs. 7.68 ± 0.43%, P < 0.001), EC ET-1 and PeNOS were greater ( P < 0.05), and EC eNOS was not different in older ( n = 23, 62 ± 1 yr) vs. young ( n = 27, 22 ± 1 yr) men. EDD was inversely related to venous EC ET-1 ( r = −0.37, P < 0.05). ET-1 receptor A inhibition with BQ-123 restored 60% of the age-related impairment in carotid artery dilation to acetylcholine in B6D2F1 mice (5–7 mo, n = 8; 30 mo, n = 11; P < 0.05). ET-1 expression is increased in vascular EC of healthy older men and is related to reduced EDD, whereas ET-1 receptor A signaling tonically suppresses EDD in old mice. Neither eNOS nor PeNOS is reduced with aging. Changes in ET-1 expression and bioactivity, but not eNOS, contribute to vascular endothelial dysfunction with aging.
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DeSouza, C. A., Shapiro, L. F., Clevenger, C. M., Dinenno, F. A., Monahan, K. D., Tanaka, H., & Seals, D. R. (2000) · Circulation · doi:10.1161/01.cir.102.12.1351 · Cited by 896 · cited 1×
“0 g dl forearm tissue 1 min (1), respectively, as described previously (9, 12, 30).”
MethodSelf-citationEskurza, I., Monahan, K. D., Robinson, J. A., & Seals, D. R. (2004) · The Journal of Physiology · doi:10.1113/jphysiol.2003.057042 · Cited by 341
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Cited by
Oxidative stress, aging, and diseases
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Wang (2012) · doi:10.1161/circresaha.111.261388 · Cited by 957
Ungvari, Z., Tarantini, S., Donato, A. J., Galvan, V., & Csiszar, A. (2018) · Circulation Research · doi:10.1161/circresaha.118.311378 · Cited by 919
Self-citationAging and vascular endothelial function in humans
Seals, D. R., Jablonski, K. L., & Donato, A. J. (2011) · Clinical Science · doi:10.1042/cs20100476 · Cited by 725
Self-citationThe Aging Cardiovascular System
Paneni, F., Diaz Cañestro, C., Libby, P., Lüscher, T. F., & Camici, G. G. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.01.064 · Cited by 618
Metadata
- Authors
- Donato, A. J., Gano, L. B., Eskurza, I., Silver, A. E., Gates, P. E., Jablonski, K., & Seals, D. R.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2009-07
- Volume
- 297
- Issue
- 1
- Pages
- H425-H432
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2169887452
- Cited by
- 316
- References
- 2
- FWCI
- 11.02
- Type
- journal article
- Language
- en
- Open access
- green
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- Donato, A. J., Gano, L. B., Eskurza, I., Silver, A. E., Gates, P. E., Jablonski, K., & Seals, D. R. (2009). Vascular endothelial dysfunction with aging: endothelin-1 and endothelial nitric oxide synthase. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00689.2008
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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