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Updated: Jan 5, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
The hypertensive potential of estrogen: An untold story
Manal Fardoun1, Hassan Dehaini2, Abdallah Shaito3
1Department of Biology, American University of Beirut, Beirut, Lebanon.
Insights
Estrogen
Area of Science:
- Endocrinology and cardiovascular research.
Background:
- Cardiovascular disease (CVD) is a leading cause of death globally.
- Estrogen's role in CVD, particularly hypertension, is complex and debated.
- While often linked to cardioprotection, estrogen may also cause vasoconstriction.
Purpose of the Study:
- To review the dual role of estrogen in regulating blood pressure.
- To explore molecular mechanisms behind estrogen's vasorelaxant and vasoconstrictive effects.
- To identify factors influencing estrogen's impact on vascular tone.
Main Methods:
- Literature review of studies on estrogen and cardiovascular function.
- Analysis of molecular pathways involving estrogen and nitric oxide synthase-1 (nNOS).
- Discussion of evidence for both vasodilatory and vasoconstrictive estrogen actions.
Main Results:
- Estrogen exhibits a "yin-yang" effect on blood pressure regulation.
- Estrogen's impact depends on the microenvironment and nNOS activity.
- Nitric oxide production leads to vasodilation, while superoxide leads to vasoconstriction.
Conclusions:
- Estrogen's role in hypertension is multifaceted, not solely protective.
- Understanding the signaling pathways is crucial for managing estrogen's cardiovascular effects.
- Further research is needed to clarify estrogen's complex influence on vascular tone.
Abstract:
Cardiovascular disease (CVD) is the major cause of morbidity and mortality worldwide. The implication of estrogen in this disease has been extensively studied. While the vast majority of published research argue for a cardioprotective role of estrogen in vascular inflammation such as in atherosclerosis, the role of estrogen in hypertension remains far from being resolved. The vasorelaxant effect of estrogen has already been well-established. However, emerging evidence supports a vasoconstrictive potential of this hormone. It has been proposed that the microenvironment dictates the effect of estrogen-induced type 1 nitric oxide synthase-1 (nNOS) on vasotone. Indeed, depending on nNOS product, nitric oxide or superoxide, estrogen can induce vasodilation or vasoconstriction, respectively. In this review, we discuss the evidence supporting the vasorelaxant effects of estrogen, and the molecular players involved. Furthermore, we shed light on recent reports revealing a vasoconstrictive role of estrogen, and speculate on the underlying signaling pathways. In addition, we identify certain factors that can account for the discrepant estrogenic effects. This review emphasizes a yin-yang role of estrogen in regulating blood pressure.
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