Oncotarget

Research Papers: Pathology:

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia

Qinqin Gao, Jiaqi Tang, Na Li, Xiuwen Zhou, Yongmei Li, Yanping Liu, Jue Wu, Yuxian Yang, Ruixiu Shi, Axin He, Xiang Li, Yingying Zhang, Jie Chen, Lubo Zhang, Miao Sun and Zhice Xu _

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Oncotarget. 2017; 8:30734-30741. https://doi.org/10.18632/oncotarget.15416

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Abstract

Qinqin Gao1,*, Jiaqi Tang1,*, Na Li1,*, Xiuwen Zhou1,*, Yongmei Li1, Yanping Liu1, Jue Wu1, Yuxian Yang1, Ruixiu Shi1, Axin He1, Xiang Li1, Yingying Zhang1, Jie Chen1, Lubo Zhang2, Miao Sun1 and Zhice Xu1,2

1 Institute for Fetology, First Hospital of Soochow University, Suzhou, China

2 Center for Perinatal Biology, Loma Linda University, Loma Linda, California, USA

* These authors have contributed equally to this work

Correspondence to:

Zhice Xu, email:

Miao Sun, email:

Keywords: preeclampsia, placenta vascular, angiotensin II, Pathology Section

Received: December 12, 2016 Accepted: February 06, 2017 Published: February 16, 2017

Abstract

The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.7% vessels in 155 tests, as referenced to KCl-induced contractions. In contrast, phenylephrine only produced contractions in 3.0% of 133 tests. In non-placental vessels, phenylephrine induced contractions in 76.0% of 67 tests, whereas angiotensin II failed to produce contractions in 75 tests. Similar results were obtained in animal placental and non-placental vessels. Compared with non-placental vessels, angiotensin II receptors and β-adrenoceptors were significantly increased in placental vessels. Compared to the vessels from normal pregnancy, angiotensin II-induced vasoconstrictions were significantly reduced in preeclamptic placentas, which was associated with a decrease in angiotensin II receptors. In addition, angiotensin II and angiotensin converting enzyme in the maternal-placenta circulation in preeclampsia were increased, whereas angiotensin I and angiotensin1-7 concentrations were unchanged. The study demonstrates a selective effect of angiotensin II in maintaining placental vessel tension, which may play an important role in development of hypertension in preeclampsia.


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