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Abstract
During pregnancy, the maternal cardiovascular system undergoes significant changes, including increased heart rate, cardiac output, plasma volume, and uteroplacental blood flow (UPBF) that are required for a successful pregnancy outcome. The increased UPBF is secondary to profound circumferential growth that extends from the downstream small spiral arteries to the upstream conduit main uterine artery. Although some of the mechanisms underlying uterine vascular remodeling are, in part, known, the factors that drive the remodeling are less clear. That higher circulating levels of estrogens are positively correlated with gestational uterine vascular remodeling suggests their involvement in this process. Estrogens binding to the estrogen receptors expressed in cytotrophoblast cells and in the uterine artery wall stimulate an outward hypertrophic remodeling of uterine vasculature. In preeclampsia, generally lower concentrations of estrogens limit the proper uterine remodeling, thereby reducing UPBF increases and restricting the growth of the fetus. This review aims to report estrogenic regulation of the maternal uterine circulatory adaptation in physiological and pathological pregnancy that favors vasodilation, and to consider the underlying molecular mechanisms by which estrogens regulate uteroplacental hemodynamics.
Highlights
Progressive and significant blood flow increases to the uterus are required for suppling adequate oxygen and nutrients for fetoplacental growth and development, and for normal pregnancy outcomes
One study showed that chronic inhibition of aromatase in the second half of baboon pregnancy significantly decreased maternal serum estrogens, uteroplacental blood flow (UPBF) and fetal growth were maintained at normal levels [133]
Estrogens may, at least in part, drive maternal uterine vascular remodeling by influencing mechanisms associated with uterine artery (UA) circumferential growth during pregnancy
Summary
Progressive and significant blood flow increases to the uterus (and placenta) are required for suppling adequate oxygen and nutrients for fetoplacental growth and development, and for normal pregnancy outcomes. In pregnant women, total maternal blood volume and cardiac output rise about 40% by term [6,7] and the uterine vessels carry up to 25% of the cardiac output vs less than 1% in the nonpregnant state [6,8]. This profound maternal physiological adaptation to pregnancy is required for a successful pregnancy in terms of both fetal and maternal wellbeing. The author reviews the estrogenic mechanisms underlying uterine vascular vasodilation and remodeling, and the evidence that estrogens participate in this process by regulating multiple mechanisms and interactive pathways
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