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Query: UMLS:C0004135 (ATM)
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The present study was undertaken in order to characterize and determine angiotensin (Ang) II receptors and renin in the porcine placenta and fetal membranes. High densities of Ang II receptors of subtype 2 (AT2 receptors) were demonstrated in all parts of the placenta and fetal membranes throughout gestation. AT1 receptors (subtype 1) were only found in the first part of the gestation and only in the allantochorion-endometrium at low densities. The total Ang II receptor density was increased in the allantochorion-endometrium in the last stage of gestation. Except for this finding the Ang II receptor density did not vary during gestation. Some of the highest receptor densities were found in the allantoamnionic membrane. The Ang II receptor densities did not correlate with the duration of the gestation in any part of the placenta. Enzymatically active renin was found in all parts of the porcine placenta and fetal membranes in concentrations similar to those found earlier in the blood plasma. The renin concentrations did not correlate with the Ang II receptor densities or the duration of the gestation in any part of the placenta. Compared with the human placenta, where the Ang II receptors are almost exclusively AT1 receptors and low receptor densities are found in the fetal membranes, the present results indicate profound species differences in the expression and function of the renin-angiotensin system in the placenta and fetal membranes.
Placenta
PMID:High densities of angiotensin II subtype 2 (AT2) receptors in the porcine placenta and fetal membranes. 873 Aug 84

Our previously published work has shown that non-ACE angiotensin II (Ang II) generating system is dominate in the placenta and may play a critical role in regulation of placental vascular contractile function. In the present study, using a collagen gel contraction assay we further studied contractility of placental vascular smooth muscle cells (VSMCs) in response to factors produced by preeclamptic (PE) placentas. Placental VSMCs/type-1 collagen gels were incubated with PE placental conditioned medium in the presence or absence of inhibitors or receptor blockers. Captopril (an ACE inhibitor), chymostatin (a non-ACE chymase inhibitor), losartan (an AT1 receptor blocker) and PD123,319 (an AT2 receptor blocker) were used to study the specific ACE vs. non-ACE and AT1 vs. AT2 effects on placental VSMC contractility, respectively. Our results showed that chymostatin, but not captopril, and PD123,319, but not losartan, significantly attenuated placental VSMC/collagen gel contraction, p<0.01, respectively. The inhibitory effects of chymostatin and PD123,319 were dose-dependent. Our results suggest that chymase, a non-ACE Ang II generating enzyme, may contribute significantly to Ang II generated in the placenta vascular tissue and that the AT2 receptor may play an important role in the regulation of Ang II induced contractility of placental VSMCs. These results provide new insights into Ang II generation and Ang II receptor regulation of vessel contractile function in the placental vasculature. These results also suggest the potential role of increased chymase activity and altered AT2 receptor function in placental related pregnancy disorders such as preeclampsia and IUGR.
Placenta 2008 Jun
PMID:Contractility of placental vascular smooth muscle cells in response to stimuli produced by the placenta: roles of ACE vs. non-ACE and AT1 vs. AT2 in placental vessel cells. 1841 9

During normal pregnancy, the renin-angiotensin system (RAS) plays a vitally important role in salt balance and subsequent well-being of mother and fetus. In this balance, one must consider not only the classical renal RAS but also that of the uteroplacental unit, where both maternal and fetal tissues contribute to the signaling cascade. Many studies have shown that in normal pregnancy there is an increase in almost all of the components of the RAS. In derangements of pregnancy this delicate equilibrium can become unbalanced. Preeclampsia is one such case. It is a disorder of pregnancy characterized by hypertension, proteinuria and placental abnormalities associated with shallow trophoblast invasion and impaired spiral artery remodeling. Despite being a leading cause of maternal death and a major contributor to maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of preeclampsia are poorly understood. Immunological mechanisms and the RAS have been long considered to be involved in the development of preeclampsia. Numerous recent studies demonstrate the presence of the angiotensin II type I receptor agonistic autoantibody (AT1-AA). This autoantibody can induce many key features of the disorder and upregulate molecules involved in the pathogenesis of preeclampsia. Here we review the functional role of the RAS during pregnancy and the impact of AT1-AA on preeclampsia.
Placenta 2008 Sep
PMID:The functional role of the renin-angiotensin system in pregnancy and preeclampsia. 1868 66