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Critical role of increased angiotensin II in the maternal placenta in a human transgenic rat model of preeclampsia
Author(s) -
Brosnihan K. Bridget,
Dechend Ralf,
Hering Lydia
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.969.10
Subject(s) - placenta , preeclampsia , endocrinology , medicine , gestation , fetus , renin–angiotensin system , angiotensin ii , andrology , pregnancy , blood pressure , biology , genetics
The pregnant female human angiotensinogen ( h AGN) transgenic rat (TGR) mated with the male h renin ( h REN) TGR has been shown to be a model of preeclampsia with increased blood pressure, proteinuria, and placenta alterations of edema and necrosis. The reverse mating of female h REN x male h AGN does not show preeclamptic features. Because the maternal influence is critical in determining whether preeclampsia occurs, we characterized the Ang peptide content of the mesometrial triangle (MT) of the maternal placenta and the fetal labyrinth placenta (Pla). Three groups of pregnant rats from the following matings [SD x SD, h RENx h AGN, and h AGNx h REN] were studied on day 21 of gestation. Animals were sedated with ether and the placentas were removed, dissected into MT and Pla, and snapfrozen until analysis. The Figure shows that Ang‐(1‐7) is the predominate peptide in the MT and Pla of both TGR pregnant groups, is signficantly increased in both TGR pregnant rats, and does not differ between maternal or fetal placenta or TGR pregnant groups. In the h AGN xh REN TGR Ang II is significantly increased in the Pla and MT, but in the h Renx h AGN Ang II is not changed in the MT. The marked contrast in the expression of Ang II in the MT of the preeclamptic model vs the non‐preeclamptic groups suggests that the maternal placenta could be critical in contributing to the preeclamptic condition. This research was supported by NHLBI P01‐HL51952.