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.

Maternal and umbilical soluble Fas concentration in normotensive and preeclamptic pregnancies

“…Preeclampsia is characterized by an increase in vascular tone, hypertension, enhanced platelet aggregation and coagulation and proteinuria, and is related to increased perinatal morbidity and mortality [4]. These changes may be related to disturbances in apoptosis.…”

sCD40 Ligand Determined in Maternal and Umbilical Cord Blood in Pregnancies Complicated by Pre-Eclampsia with and without Intrauterine Growth Retardation

“…Pregnant patients with pre-eclampsia, apart from increased vascular tone, hypertension, proteinuria, enhanced platelet aggregation and decreased intravascular volume due to increased endothelial permeability, reveal pathological changes due to decreased perfusion in many organs (uterus, kidney, brain, placenta) [30] . Disturbances in vascular endothelium and in placental and uteroplacental vascular system development might be the primary cause of pre-eclampsia.…”

Local Renin-Angiotensin System in the Reproductive System

“…Although the role of the RAS concerning invasion of trophoblast and placentation is poorly investigated, there is evidence that dysfunction of this system may cause hypertension and preeclampsia (56, 72, 73, 74): patients with preeclampsia present with increased expression of Angiotensin II and AT1R in maternal decidua cells and in the placenta itself (74, 75). In pre-eclamptic pregnancies Angiotensin II and AT1R was been observed to be increased, whereas levels of Angiotensin I, Angiotensin (1–7), ACE, and ACE2 were normal as compared to healthy pregnancies (48).…”