Journal
VASCULAR PHARMACOLOGY
Volume 124, Issue -, Pages -Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.vph.2019.106600
Keywords
Blood pressure; Estrogen; 17 beta-estradiol; Hypertension; Vasoconstriction; Vasodilation; Vascular smooth muscle cells
Categories
Funding
- American University of Beirut-Faculty of Medicine [320133]
- National Center for Scientific Research (CNRS)
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available