New conception for the development of hypertension in preeclampsia

// Qinqin Gao 1,* , Jiaqi Tang 1,* , Na Li 1,* , Xiuwen Zhou 1,* , Xiaolin Zhu 1 , Weisheng Li 1 , Bailin Liu 1 , Xueqin Feng 1 , Jianying Tao 1,3 , Bing Han 3 , Hong Zhang 3 , Miao Sun 1 and Zhice Xu 1,2 1 Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China 2 Center for Perinatal Biology, Loma Linda University, California, USA 3 Department of Obstetrics and Gynecology, First and Second Affiliated Hospital of Soochow University, Municipal Hospital, Suzhou, China * These authors have contributed equally to this work Correspondence to: Zhice Xu, email: // Miao Sun, email: // Keywords : nitric oxide, cGMP/sGC pathway, vascular dysfunction, placenta, preeclampsia, Pathology Section Received : August 10, 2016 Accepted : November 14, 2016 Published : November 16, 2016 Abstract Placental vascular dysfunction was suggested to be critical for placental ischemia-initiated hypertension in preeclampsia, although the contributions of endothelium involved are unclear. The present study found, unlike non-placental vessels, acetylcholine showed no vasodilatation effect on placental vessels, indicating that endothelial-derived nitric oxide (NO) was extremely weak in placental vessels. Placental vascular responses to exogenous NO from sodium nitroprusside (SNP) were significantly different from non-placental vessels. These results were further confirmed in sheep, and rat vessels. In preeclamptic placental vessels, acetylcholine also showed no vasodilatation effects, while vascular responses to SNP were suppressed, associated with impaired cGMP/sGC pathway in vascular smooth muscle cells (VSMCs). The current theory on placental ischemia-initiated hypertension in preeclampsia focused on changes in placental vascular functions, including endothelial dysfunction. This study found the placental endothelium contributed very poorly to vasodilatation, and altered vascular functions in preeclampsia mainly occurred in VSMCs instead of endothelial cells. The findings contribute importantly to understanding the special feature of placental vascular functions and its pathophysiological changes in the development of hypertension in preeclampsia.