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Cited by 291

The DOI matches its Crossref record; 107 of the 107 references it cites were found in a registry or an index.

Gender and the renin–angiotensin–aldosterone system

Komukai, Kimiaki, Mochizuki, Seibu, Yoshimura, Michihiro·2010·Fundamental & Clinical Pharmacology

Abstract

Premenopausal women are protected to some extent from cardiovascular and kidney diseases. Because this protection weakens after menopause, sex hormones are believed to play an important role in the pathogenesis of cardiovascular and kidney diseases. The cardiovascular system and the kidneys are regulated by the renin–angiotensin–aldosterone system (RAAS), which in turn, appears to be regulated by sex hormones. In general, oestrogen increases angiotensinogen levels and decreases renin levels, angiotensin‐converting enzyme (ACE) activity, AT 1 receptor density, and aldosterone production. Oestrogen also activates counterparts of the RAAS such as natriuretic peptides, AT 2 receptor density, and angiotensinogen (1‐7). Progesterone competes with aldosterone for mineralocorticoid receptor. Less is known about androgens, but testosterone seems to increase renin levels and ACE activity. These effects of sex hormones on the RAAS can explain at least some of the gender differences in cardiovascular and kidney diseases.

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Metadata

Authors
Komukai, K., Mochizuki, S., & Yoshimura, M.
Venue
Fundamental & Clinical Pharmacology
Publisher
Wiley
Published
2010-11-11
Volume
24
Issue
6
Pages
687-698
ISSN
  • 0767-3981 (ISSN-L)
  • 1472-8206
OpenAlex
W1509779962
Cited by
291
References
107
FWCI
6.54
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Gender and the renin–angiotensin–aldosterone system. https://app.cochat.ai/papers/10.1111/j.1472-8206.2010.00854.x
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Komukai, K., Mochizuki, S., & Yoshimura, M. (2010). Gender and the renin–angiotensin–aldosterone system. Fundamental & Clinical Pharmacology. https://doi.org/10.1111/j.1472-8206.2010.00854.x

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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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