Effects of estrogen on the vascular system
Open accessAbstract
The cardiovascular protective actions of estrogen are partially mediated by a direct effect on the vessel wall. Estrogen is active both on vascular smooth muscle and endothelial cells where functionally competent estrogen receptors have been identified. Estrogen administration promotes vasodilation in humans and in experimental animals, in part by stimulating prostacyclin and nitric oxide synthesis, as well as by decreasing the production of vasoconstrictor agents such as cyclooxygenase-derived products, reactive oxygen species, angiotensin II, and endothelin-1. In vitro, estrogen exerts a direct inhibitory effect on smooth muscle by activating potassium efflux and by inhibiting calcium influx. In addition, estrogen inhibits vascular smooth muscle cell proliferation. In vivo, 17beta-estradiol prevents neointimal thickening after balloon injury and also ameliorates the lesions occurring in atherosclerotic conditions. As is the case for other steroids, the effect of estrogen on the vessel wall has a rapid non-genomic component involving membrane phenomena, such as alteration of membrane ionic permeability and activation of membrane-bound enzymes, as well as the classical genomic effect involving estrogen receptor activation and gene expression.
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Estrogen induces upregulation of NO production in the endothelium via non-genomic activation of second messengers like Ca2+ cAMP.
“Estrogen induces upregulation of NO production in the endothelium via multiple mechanisms, including genomic (stimulation of NO synthase gene expression) and non-genomic activation of second messengers like Ca2+ cAMP [171].”
From Temperature regulation in women: Effects of the menstrual cycle (2020) · cites this paper as [171]
Estrogen promotes vasodilation in part by stimulating nitric oxide (NO) and prostacyclin synthesis.
“Estrogen promotes vasodilation in part by stimulating nitric oxide (NO) and prostacyclin synthesis, and inhibits vasoconstriction by decreasing the production of vasoconstrictors like cyclooxygenase-derived products, angiotensin II, and endothelin-1 [171].”
From Temperature regulation in women: Effects of the menstrual cycle (2020) · cites this paper as [171]
Estrogen inhibits vasoconstriction by decreasing the production of vasoconstrictors like cyclooxygenase-derived products, angiotensin II, and endothelin-1.
“Estrogen promotes vasodilation in part by stimulating nitric oxide (NO) and prostacyclin synthesis, and inhibits vasoconstriction by decreasing the production of vasoconstrictors like cyclooxygenase-derived products, angiotensin II, and endothelin-1 [171].”
From Temperature regulation in women: Effects of the menstrual cycle (2020) · cites this paper as [171]
Estrogen induces upregulation of NO production in the endothelium via genomic mechanisms, including stimulation of NO synthase gene expression.
“Estrogen induces upregulation of NO production in the endothelium via multiple mechanisms, including genomic (stimulation of NO synthase gene expression) and non-genomic activation of second messengers like Ca2+ cAMP [171].”
From Temperature regulation in women: Effects of the menstrual cycle (2020) · cites this paper as [171]
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References 60 · Cited by 213
Research works printed but not linked: 4
- Costa SG, Anversa P, Scavone C, Sucupira M & Carvalho MHC (1998). Nitric oxide synthase activity in microvessels of SHR and normotensive rats: effects of estrogen. Journal of Hypertension, 25: S80 (Abstract).
- Ergul A, Shoemaker K, Puett D & Tackett RL (1998). Gender differ- ences in the expression of endothelin receptors in human saphen- ous vein in vitro. Journal of Pharmacology and Experimental Thera- peutics, 285: 511-517.
- Writing Group for the Women's Health Initiative Investigators (2002). Risks and benefits of estrogen plus progestin in healthy postmenopausal women. Journal of the American Medical Associa- tion, 288: 321-333.
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- Authors
- Tostes, R. C., Nigro, D., Fortes, Z. B., & Carvalho, M. H. C.
- Affiliations
- Universidade de São Paulo (BR)
- ORCID
- Tostes, R.C.
- Venue
- Brazilian Journal of Medical and Biological Research
- Publisher
- FapUNIFESP (SciELO)
- Published
- 2003-09
- Volume
- 36
- Issue
- 9
- Pages
- 1143-1158
- ISSN
- 0100-879X (ISSN-L)
- OpenAlex
- W1964811030
- Cited by
- 213
- References
- 60
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 10 · 2023: 10 · 2022: 8 · 2021: 9 · 2020: 19 · 2019: 5 · 2018: 10 · 2017: 5 · 2016: 15 · 2015: 10 · 2014: 11 · 2013: 10 · 2012: 12
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Brazilian Journal of Medical and Biological Research (publishedVersion, cc-by)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
- Americanae (AECID Library) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Fundação de Amparo à Pesquisa do Estado de São Paulo (00/12141-8, 00/04611-4, 97/14208-8)
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Menopause: Health Impacts and Treatments
- Keywords
- estrogen, cardioprotection, vascular smooth muscle, endothelial cells, estrogen receptor, vasodilation, prostacyclin, nitric oxide, vasoconstrictors, angiotensin II, endothelin-1, potassium efflux, calcium influx, smooth muscle cell proliferation, neointimal thickening, atherosclerosis, non-genomic estrogen effects
- MeSH terms
- Cardiovascular System, Endothelium, Vascular, Estrogens, Humans, Muscle, Smooth, Vascular
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