title: Comparative analysis of the angiotensin-II receptor in placental vascular endothelial cells in preeclamptic and normotensive patients.
abstract: The aim of this study was to compare the immunoreactivity of angiotensin-II receptor type 1 (AT1R) in the vascular endothelial cells of human placental vessels in normal and preeclamptic pregnancies. Immunohistochemistry was used to examine the localization of AT1R in the vascular endothelium of human placental vessels. In preeclamptic patients without intrauterine growth retardation (IUGR) the mean histological index H score was significantly higher, but significantly decreased in patients with preeclampsia complicated by IUGR in comparison with the control group. Immunolocalization of AT1R in vascular endothelial cells in our study supports the view that angiotensin II may play a role in the regulation of vascular tone and vascular resistance and the actions of other vasoactive factors, vasodilators or vasoconstrictors. However, our results confirmed that AT1R immunoreactivity is elevated in vascular endothelial cells of human placenta from pregnancies complicated by preeclampsia, suggesting a higher activity of the renin-angiotensin-aldosterone system (RAAS) in women with preeclampsia. On the other hand reduced immunoreactivity of AT1R in placental vascular endothelial cells in pregnancy complicated by preeclampsia with IUGR may result from chronic higher RAAS activity and may suggest the decreased ability to compensate and the inability to restore the normal balance between vasodilators and vasoconstrictors. These results may also reflect destructive changes and dysfunction of the vascular endothelium in preeclamptic pregnancy with IUGR.
authors.affiliation: Department of Obstetrics and Perinatology, University School of Medicine, Jaczewskiego 8, PL-20-950 Lublin, Poland. marzena@asklepios.am.lublin.pl
authors.forename: Marzena
authors.initials: M
authors.lastname: Laskowska
authors.forename: Gavin P
authors.initials: GP
authors.lastname: Vinson
authors.forename: Justyna
authors.initials: J
authors.lastname: Szumiło
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Laskowska
authors.forename: Bozena
authors.initials: B
authors.lastname: Leszczyńska-Gorzelak
authors.forename: Jan
authors.initials: J
authors.lastname: Oleszczuk
mesh_terms: D000450:Aldosterone / Q000502:physiology; D000804:Angiotensin II / Q000097:blood; D001034:Apgar Score; D001724:Birth Weight; D001794:Blood Pressure; D042783:Endothelial Cells / Q000737:chemistry*; D005260:Female; D005313:Fetal Death; D005317:Fetal Growth Retardation / Q000150:complications / Q000378:metabolism; D005865:Gestational Age; D006801:Humans; D007150:Immunohistochemistry; D010920:Placenta / Q000098:blood supply*; D011225:Pre-Eclampsia / Q000150:complications / Q000378:metabolism*; D011247:Pregnancy; D044140:Receptor, Angiotensin, Type 1 / Q000032:analysis*; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D000450:Aldosterone