The Uterine Placental Bed Renin-Angiotensin System in Normal and Preeclamptic Pregnancy

Author:

Anton Lauren1,Merrill David C.2,Neves Liomar A. A.1,Diz Debra I.1,Corthorn Jenny3,Valdes Gloria3,Stovall Kathryn1,Gallagher Patricia E.1,Moorefield Cheryl2,Gruver Courtney2,Brosnihan K. Bridget1

Affiliation:

1. Hypertension and Vascular Research Center (L.A., L.A.A.N., D.I.D., K.S., P.E.G., K.B.B.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157

2. Department of Obstetrics and Gynecology (D.C.M., C.M., C.G.), Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157

3. Departamentos Nefrología y Obstetricia/Ginecología (J.C., G.V.), Facultad Medicina Universidad Católica, Santiago, 8320000 Chile

Abstract

Abstract Previously, we demonstrated activation of the renin-angiotensin system in the fetal placental chorionic villi, but it is unknown whether the immediately adjacent area of the maternal uterine placental bed is regulated similarly. This study measured angiotensin peptides, renin-angiotensin system component mRNAs, and receptor binding in the fundus from nonpregnant subjects (n = 19) and in the uterine placental bed from normal (n = 20) and preeclamptic (n = 14) subjects. In the uterine placental bed from normal pregnant women, angiotensin II peptide levels and angiotensinogen, angiotensin-converting enzyme, angiotensin receptor type 1 (AT1), AT2, and Mas mRNA expression were lower as compared with the nonpregnant subjects. In preeclamptic uterine placental bed, angiotensin II peptide levels and renin and angiotensin-converting enzyme mRNA expression were significantly higher than normal pregnant subjects. The AT2 receptor was the predominant receptor subtype in the nonpregnant fundus, whereas all angiotensin receptor binding was undetectable in normal and preeclamptic pregnant uterine placental bed compared with nonpregnant fundus. These findings suggest that the maternal uterine placental bed may play an endocrine role by producing angiotensin II, which acts in the adjacent placenta to vasoconstrict fetal chorionic villi vessels where we have shown previously that AT1 receptors predominate. This would lead to decreased maternal-fetal oxygen exchange and fetal nutrition, a known characteristic of preeclampsia.

Publisher

The Endocrine Society

Subject

Endocrinology

Reference39 articles.

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2. Fisher SJ, Roberts JM 1999 Defects in placentation and placental perfusion. In: Linheimer M, Roberts JM, Cunningham FG, eds. Chesley’s hypertensive disorders in pregnancy. 2nd ed. Stanford, CA: Appleton, Lange; 377–394

3. Pathophysiology of preeclampsia: linking placental ischemia/hypoxia with microvascular dysfunction.;Granger;Microcirculation,2002

4. Taylor RN, Roberts JM 1999 Endothelial cell dysfunction. In: Linheimer M, Roberts JM, Cunningham FG, eds. Chesley’s hypertensive disorders in pregnancy. 2nd ed. Stanford, CA: Appleton, Lange; 395–429

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