title: The uterine placental bed Renin-Angiotensin system in normal and preeclamptic pregnancy.
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 (AT(1)), AT(2), 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 AT(2) 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 AT(1) receptors predominate. This would lead to decreased maternal-fetal oxygen exchange and fetal nutrition, a known characteristic of preeclampsia.
authors.affiliation: Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston Salem, North Carolina 27157-1032, USA.
authors.forename: Lauren
authors.initials: L
authors.lastname: Anton
authors.forename: David C
authors.initials: DC
authors.lastname: Merrill
authors.forename: Liomar A A
authors.initials: LA
authors.lastname: Neves
authors.forename: Debra I
authors.initials: DI
authors.lastname: Diz
authors.forename: Jenny
authors.initials: J
authors.lastname: Corthorn
authors.forename: Gloria
authors.initials: G
authors.lastname: Valdes
authors.forename: Kathryn
authors.initials: K
authors.lastname: Stovall
authors.forename: Patricia E
authors.initials: PE
authors.lastname: Gallagher
authors.forename: Cheryl
authors.initials: C
authors.lastname: Moorefield
authors.forename: Courtney
authors.initials: C
authors.lastname: Gruver
authors.forename: K Bridget
authors.initials: KB
authors.lastname: Brosnihan
mesh_terms: D000409:Alanine / Q000494:pharmacology; D000803:Angiotensin I / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism; D000085962:Angiotensin-Converting Enzyme 2; D015536:Down-Regulation; D005260:Female; D015870:Gene Expression; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D010446:Peptide Fragments / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D010920:Placenta / Q000378:metabolism*; D011225:Pre-Eclampsia / Q000378:metabolism*; D011247:Pregnancy / Q000378:metabolism*; D011725:Pyridines / Q000494:pharmacology; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000187:drug effects / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*; D013237:Stereoisomerism; D014599:Uterus / Q000378:metabolism*
chemical_list: D007093:Imidazoles; D010446:Peptide Fragments; D011725:Pyridines; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D000804:Angiotensin II; C073402:PD 123319; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; C000705307:ACE2 protein, human; D000085962:Angiotensin-Converting Enzyme 2; C118790:angiotensin I (1-7); D019808:Losartan; D000409:Alanine