title: New conception for the development of hypertension in preeclampsia.
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.
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Qinqin
authors.initials: Q
authors.lastname: Gao
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Jiaqi
authors.initials: J
authors.lastname: Tang
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Na
authors.initials: N
authors.lastname: Li
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Xiuwen
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Xiaolin
authors.initials: X
authors.lastname: Zhu
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Weisheng
authors.initials: W
authors.lastname: Li
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Bailin
authors.initials: B
authors.lastname: Liu
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Xueqin
authors.initials: X
authors.lastname: Feng
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.|Department of Obstetrics and Gynecology, First and Second Affiliated Hospital of Soochow University, Municipal Hospital, Suzhou, China.
authors.forename: Jianying
authors.initials: J
authors.lastname: Tao
authors.affiliation: Department of Obstetrics and Gynecology, First and Second Affiliated Hospital of Soochow University, Municipal Hospital, Suzhou, China.
authors.forename: Bing
authors.initials: B
authors.lastname: Han
authors.affiliation: Department of Obstetrics and Gynecology, First and Second Affiliated Hospital of Soochow University, Municipal Hospital, Suzhou, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Sun
authors.affiliation: Institute for Fetology, First Affiliated Hospital of Soochow University, Suzhou, China.|Center for Perinatal Biology, Loma Linda University, California, USA.
authors.forename: Zhice
authors.initials: Z
authors.lastname: Xu
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D016022:Case-Control Studies; D006152:Cyclic GMP / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010920:Placenta / Q000098:blood supply*; D011225:Pre-Eclampsia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D011247:Pregnancy; D017207:Rats, Sprague-Dawley; D034561:Sheep, Domestic; D000071756:Soluble Guanylyl Cyclase / Q000378:metabolism; D014469:Umbilical Arteries / Q000378:metabolism / Q000503:physiopathology; D014471:Umbilical Veins / Q000378:metabolism / Q000503:physiopathology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009569:Nitric Oxide; D000071756:Soluble Guanylyl Cyclase; D006152:Cyclic GMP
keywords: Pathology Section; cGMP/sGC pathway; nitric oxide; placenta; preeclampsia; vascular dysfunction