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Updated: Aug 2, 2026
Ovariectomy and 17β-estradiol Replacement in Rats and Mice: A Visual Demonstration
Published on: June 7, 2012
The heart as a target for oestrogens
L Brown1, I Hoong, S A Doggrell
1Department of Physiology and Pharmacology, The University of Queensland, Australia. brown@plpk.uq.edu.au
Insights
Estrogen therapy in postmenopausal women shows reduced cardiovascular disease risk in observational studies, but clinical trials indicate increased coronary events. Further research is needed.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Pharmacology
Background:
- Observational studies suggest estrogen reduces cardiovascular disease (CVD) risk in postmenopausal women.
- Estrogens impact blood lipids and cardiovascular system regulators, potentially lowering CVD risk.
- The heart possesses functional estrogen receptors in vasculature, myocytes, and fibroblasts.
Purpose of the Study:
- To review mechanisms of estrogen's physiological effects on healthy and diseased hearts.
- To reconcile conflicting findings between observational and randomized controlled trials of estrogen therapy for CVD.
- To identify future research directions for estrogen-based cardiovascular risk reduction.
Main Methods:
- Literature review of observational studies and randomized controlled trials (RCTs).
- Analysis of proposed rapid and long-term mechanisms of estrogen action on cardiovascular tissues.
- Evaluation of clinical trial data regarding estrogen and progestin effects on coronary events and atherosclerosis.
Main Results:
- Estrogens exert rapid effects like vasodilation and anti-arrhythmic actions, and longer-term effects including nitric oxide synthase induction.
- Conflicting evidence exists: observational studies show reduced CVD risk, while RCTs (e.g., WHI) indicate increased coronary events, particularly early on.
- Estrogen's effect on fibroblasts varies: promoting growth in non-proliferating cells but inhibiting proliferation in others.
Conclusions:
- Estrogen's cardiovascular effects are complex, with rapid and long-term actions on various cardiac components.
- Clinical trial data challenge the protective role of combined estrogen and progestin therapy in postmenopausal women with existing heart disease.
- Further studies in animal models and clinical trials with selective estrogen receptor modulators (SERMs) are warranted to clarify estrogen's role in cardiovascular risk reduction for both sexes.
Abstract:
Observational studies have consistently shown a markedly decreased risk of cardiovascular disease in postmenopausal women when treated with oestrogens. This review discusses plausible mechanisms for the physiological effects of oestrogens in healthy and diseased hearts. Oestrogens have well-documented effects on blood lipids and the regulators of the cardiovascular system, which should reduce risk. In addition, the heart is a primary target for oestrogens with functional oestrogen receptors in the coronary vasculature and on cardiac myocytes and fibroblasts. Rapid oestrogen effects include vasodilatation and anti-arrhythmic effects by actions on ion channels, and some of these effects may be pharmacological rather than physiological. Longer term responses to physiological levels of oestrogen include an increased expression of nitric oxide synthase in myocytes and endothelial cells as well as proinflammatory and pro-arrhythmic effects. Oestrogens induce growth of non-proliferating fibroblasts but inhibit the replication of proliferating fibroblasts. In contrast to the observational studies, two randomised, controlled studies of oestrogen and progestins in postmenopausal women with coronary heart disease have now shown increased coronary events, especially in the first year of study, and no change in the progression of coronary atherosclerosis. Further studies of the complex effects of oestrogens on healthy and diseased animal models are essential. Large clinical trials of the newer selective oestrogen receptor modulators to lower cardiovascular risk in both males and females should be considered as a priority.
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