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Estrogen status and the renin angiotensin aldosterone system
journal contribution
posted on 2016-03-18, 11:05 authored by Emma ODonnellEmma ODonnell, John S. Floras, Paula J. HarveyThe renin-angiotensin-aldosterone system (RAAS) is integrally involved in multiple cardiovascular physiological processes including arterial blood pressure (BP) regulation. Over activity of the RAAS has been implicated in the pathogenesis of a number of cardiovascular disease entities, including hypertension. Several lines of evidence suggest estrogen favorably modulates the RAAS. Conversely, estrogen deficiency due to menopause may contribute to over activity of the RAAS. Of importance, estrogen deficiency in women is not exclusive to the postmenopausal period. Functional hypothalamic amenorrhea is a reversible cause of premenopausal hypoestrogenemia. In contrast to postmenopausal women (PMW), premenopausal women with exercise-associated functional hypothalamic amenorrhea demonstrate decreased, not increased, resting BP compared with their estrogen-replete eumenorrheic counterpart. In this review we briefly examine the effects of estrogen status on the RAAS and present the hypothesis that the RAAS is altered in physically active women with functional hypothalamic amenorrhea.
History
School
- Sport, Exercise and Health Sciences
Published in
American journal of physiology. Regulatory, integrative and comparative physiologyVolume
307Issue
5Pages
R498 - R500Citation
O'DONNELL, E., FLORAS, J.S. and HARVEY, P.J., 2014. Estrogen status and the renin angiotensin aldosterone system. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 307(5), pp. R498-R500.Publisher
© American Physiological SocietyVersion
- VoR (Version of Record)
Publisher statement
This work is made available according to the conditions of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. Full details of this licence are available at: https://creativecommons.org/licenses/by-nc-nd/4.0/Publication date
2014Notes
This paper is in closed access.ISSN
0363-6119eISSN
1522-1490Publisher version
Language
- en