The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Hormonal modulation of endothelial NO production
Open accessAbstract
Since the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely circulating chemical factors that impact production of NO both by rapid effects on the activity of endothelial nitric oxide synthase (eNOS) through phosphorylation of the enzyme and longer term modulation through changes in amount of eNOS protein. Hormones that increase NO production including estrogen, progesterone, insulin, and growth hormone do so through both of these common mechanisms. In contrast, some hormones, including glucocorticoids, progesterone, and prolactin, decrease NO bioavailability. Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals. Feedback regulation by the hormones themselves as well as the ability of NO to regulate hormonal release provides a second level of complexity that can also contribute to changes in NO levels. These effects on eNOS and changes in NO production may contribute to variability in risk factors, presentation of and treatment for cardiovascular disease associated with aging, pregnancy, stress, and metabolic disorders in men and women.
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Cites
Oxidative Stress and Vascular Disease
Madamanchi, N. R., Vendrov, A., & Runge, M. S. (2005) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000150649.39934.13 · Cited by 1,618 · cited 1×
“Since free radicals such as superoxide may inactivate NO, the ability of estrogen to suppress superoxide production could also help to increase endotheliumdependent vasodilatation [51].”
Cusi, K., Maezono, K., Osman, A., Pendergrass, M., Patti, M. E., Pratipanawatr, T., DeFronzo, R. A., Kahn, C. R., & Mandarino, L. J. (2000) · Journal of Clinical Investigation · doi:10.1172/jci7535 · Cited by 1,139
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“Given the important role of eNOS in contributing to the physiological effects of insulin, what is the impact of insulin resistance on endothelial function and vice versa? Interestingly, in both humans [13] and in animal models of insulin resistance [36], there is a specific impairment of PI3Kdependent signaling pathwa…”
Sex difference in resting pituitary-adrenal function in the rat
Critchlow, V., Liebelt, R. A., Bar-Sela, M., Mountcastle, W., & Lipscomb, H. S. (1963) · American Journal of Physiology-Legacy Content · doi:10.1152/ajplegacy.1963.205.5.807 · Cited by 499
Modulation of Antioxidant Enzyme Expression and Function by Estrogen
Strehlow, K., Rotter, S., Wassmann, S., Adam, O., Grohé, C., Laufs, K., Böhm, M., & Nickenig, G. (2003) · Circulation Research · doi:10.1161/01.res.0000082334.17947.11 · Cited by 483 · cited 1×
“For example, estrogen has been shown to suppress oxidative stress by a variety of mechanisms [37, 61, 89, 90].”
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“The ability of insulin to cause vasodilatation is not merely a consequence of changes in carbohydrate metabolism [97].”
Acute Effects of Growth Hormone on Vascular Function in Human Subjects
Napoli, R., Guardasole, V., Angelini, V., D’Amico, F., Zarra, E., Matarazzo, M., & Saccà, L. (2003) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2003-030144 · Cited by 74
Cited by
Mechanistic Pathways of Sex Differences in Cardiovascular Disease
Regitz-Zagrosek, V., & Kararigas, G. (2017) · Physiological Reviews · doi:10.1152/physrev.00021.2015 · Cited by 732
Vascular endothelium – Gatekeeper of vessel health
Cahill, P. A., & Redmond, E. M. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.03.007 · Cited by 518
Estrogen and the cardiovascular system
Knowlton, A. A., & Lee, A. R. (2012) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2012.03.007 · Cited by 489
Nitric Oxide Signaling and Regulation in the Cardiovascular System: Recent Advances
Carlström, M., Weitzberg, E., & Lundberg, J. O. (2024) · Pharmacological Reviews · doi:10.1124/pharmrev.124.001060 · Cited by 103
Why the endothelium? The endothelium as a target to reduce diabetes-associated vascular disease
Triggle, C. R., Ding, H., Marei, I., Anderson, T. J., & Hollenberg, M. D. (2020) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2019-0677 · Cited by 49
Metadata
- Authors
- Duckles, S. P., & Miller, V. M.
- Venue
- Pflügers Archiv - European Journal of Physiology
- Published
- 2010-03-07
- Volume
- 459
- Issue
- 6
- Pages
- 841-851
- ISSN
- 0031-6768 (ISSN-L)
- 1432-2013
- OpenAlex
- W2063449352
- Cited by
- 175
- References
- 7
- FWCI
- 7.61
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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