Estrogen Reduces Aldosterone, Upregulates Adrenal Angiotensin II AT2 Receptors and Normalizes Adrenomedullary Fra-2 in Ovariectomized Rats
Open accessAbstract
We studied the effect of ovariectomy and estrogen replacement on expression of adrenal angiotensin II AT 1 and AT 2 receptors, aldosterone content, catecholamine synthesis, and the transcription factor Fos-related antigen 2 (Fra-2). Ovariectomy increased AT 1 receptor expression in the adrenal zona glomerulosa and medulla, and decreased adrenomedullary catecholamine content and Fra-2 expression when compared to intact female rats. In the zona glomerulosa, estrogen replacement normalized AT 1 receptor expression, decreased AT 1B receptor mRNA, and increased AT 2 receptor expression and mRNA. Estrogen treatment decreased adrenal aldosterone content. In the adrenal medulla, the effects of estrogen replacement were: normalized AT 1 receptor expression, increased AT 2 receptor expression, AT 2 receptor mRNA, and tyrosine hydroxylase mRNA, and normalized Fra-2 expression and catecholamine content. We demonstrate that the constitutive adrenal expression of AT 1 receptors, catecholamine synthesis and Fra-2 expression are partially under the control of reproductive hormones. Our results suggest that estrogen treatment decreases aldosterone production through AT 1 receptor downregulation and AT 2 receptor upregulation. AT 2 receptor upregulation and modulation of Fra-2 expression may participate in the estrogen-dependent normalization of adrenomedullary catecholamine synthesis in ovariectomized rats. The AT 2 receptor upregulation and the decrease in AT 1 receptor function and in the production of the fluid-retentive, pro-inflammatory hormone aldosterone partially explain the protective effects of estrogen therapy.
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E2 inhibits AngII-stimulated aldosterone secretion in vitro.
“E2 also inhibits AngII-stimulated aldosterone secretion in vitro [ 48 , 106 , 133 ]”
From Sex differences in potassium regulation: evidence, molecular mechanisms and clinical implications (2026) · cites this paper as [133]
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- Authors
- Macova, M., Armando, I., Zhou, J., Baiardi, G., Tyurmin, D., Larrayoz-Roldan, I. M., & Saavedra, J. M.
- Affiliations
- National Institutes of Health (US)
- Venue
- Neuroendocrinology
- Publisher
- S. Karger AG
- Published
- 2008
- Volume
- 88
- Issue
- 4
- Pages
- 276-286
- ISSN
- 0028-3835 (ISSN-L)
- 1423-0194
- PMC
- PMC2677380
- OpenAlex
- W2000398122
- Cited by
- 75
- References
- 75
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 5 · 2023: 8 · 2022: 4 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 3 · 2017: 4 · 2016: 7 · 2015: 2 · 2014: 1 · 2013: 3 · 2012: 5
- FWCI
- 0.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Americanae (AECID Library) (publishedVersion, other-oa)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
- Funders
- National Institutes of Health (Z99 MH999999)
- National Institute of Mental Health (Z01MH002762)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Keywords
- estrogen, ovariectomy, estrogen replacement therapy, angiotensin II type 1 receptor, angiotensin II type 2 receptor, aldosterone, adrenal zona glomerulosa, adrenal medulla, catecholamine synthesis, tyrosine hydroxylase, reproductive hormones, estrogen therapy
- MeSH terms
- Adrenal Medulla, Aldosterone, Animals, Catecholamines, Estrogens, Female, Ovariectomy, RNA, Messenger, Tyrosine 3-Monooxygenase, Zona Glomerulosa, Estrogen Replacement Therapy, Rats, Wistar, Models, Animal, Receptor, Angiotensin, Type 2, Receptor, Angiotensin, Type 1, Rats, Fos-Related Antigen-2
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