Current Topic: The Uteroplacental Renin–Angiotensin System

Nielsen, Arne Høj; Schauser, Kirsten; Poulsen, Knud

doi:10.1053/plac.2000.0535

Cited by 129 publications

(126 citation statements)

References 90 publications

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“…The placenta produces ANG II [12][13][14][15][16], TX [17,18] and ET [19][20][21]. To study which vasoactivators and their pathways produced by PE placenta were more responsible for regulating the vasomotor response in the placental vasculature, selected receptor antagonists or inhibitors of three major vasoconstrictors, ANG II, TX and ET-1, were used.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have demonstrated that ANG I [13] and ANG II [39] are present in the placenta and the uteroplacental unit possesses all components of the RAS necessary for their generation [12]; renin [14], angiotensin [40] and ACE [15]. However, the impact of the altered RAS on the fetal side of the placenta is not well defined [41,42].…”

Section: Discussionmentioning

confidence: 99%

“…Past studies have described that placental tissues produce ANG II [12][13][14][15][16], TX [17,18] and ET [19][20][21] and they are major contributors to the vasoconstriction in PE. Receptors for ANG II [2,6,[22][23][24][25], TX [26,27], and ET [28] are present in placental trophoblasts and vasculature.…”

Section: Introductionmentioning

confidence: 99%

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Vasoreactivity of Chorionic Plate Arteries in Response to Vasoconstrictors Produced by Preeclamptic Placentas

2007

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Inadequate blood flow and increased vasoconstriction of the placenta contribute to pregnancy associated disorders such as preeclampsia (PE). Because placental vessels lack autonomic innervation, humoral effects of the placenta must play critical roles in regulation of fetal-placental vascular contractility. In this study, we examined the nature of humoral factors produced by PE trophoblasts on placental vessel contractility using an organ bath perfusion model. Vasomotor responses were studied in vitro using placental chorionic plate arteries. Vessel rings from third branch chorionic plate arteries were dissected from human placentas following normal or PE delivery. The arterial rings were equilibrated in Krebs Henseleit buffer and exposed to placental conditioned medium, which was prepared by culture of villous tissue from PE placentas. Receptor antagonists for angiotensin II (ANG II), thromboxane (TX), and endothelin (ET) were used to determine which humoral factor produced by placental tissue (trophoblasts) was more effective in promoting vasoconstriction. The role of angiotensin converting enzyme (ACE) and non-ACE ANG II generating enzymes in regulation of placental vasomotor tone were also investigated. A total of 80 arterial rings from 48 placentas were studied. Our results showed: 1) enhanced vasomotor tone in arteries from PE placentas compared to those from normal placentas; 2) PE-CM induced vaso-constrictive activity could be partially attenuated by receptor antagonists for TX, ANG II and ET, respectively; and 3) chymostatin (a chymase inhibitor) produced a stronger inhibitory effect than captopril (ACE inhibitor) on PE conditioned medium induced vasoconstriction. Our data demonstrate increased vasocontractility in PE placentas and suggest that the non-ACE pathway is probably a major source of ANG II produced in the human placenta.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Vasoreactivity of Chorionic Plate Arteries in Response to Vasoconstrictors Produced by Preeclamptic Placentas

2007

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“…Placental tissues are not only able to produce various vasoactive agents, like angiotensin II (Ang II) [1][2][3], thromboxane (TX) [4][5][6], and endothelin (ET) [7,8], but also possess receptors for each of these vasoactivators, which ensure that the placental vasomotor activity is controlled in both the autocrine and/or the paracrine fashions. Using an organ bath perfusion model, we recently demonstrated that vasoconstrictors produced by preeclamptic placentas could induce constriction of chorionic plate arteries [9].…”

Section: Introductionmentioning

confidence: 99%

“…Strikingly, the open reading frame of trophoblast chymase gene is 100% homologous to that reported in the human heart [10,12], suggesting chymase may play an important role in Ang II generation and regulation of placental vascular reactivity during pregnancy. Ang I and Ang II are present in the placenta, and the uteroplacental unit possesses all necessary components of the renin-angiotensin-system (RAS) [1,3]. However, the specificities of ACE and non-ACE Ang II generating enzymes and Ang II receptors in regulation of placental vessel cell contractility have not been well studied.…”

Section: Introductionmentioning

confidence: 99%

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

Benoit

Zhang

et al. 2008

Placenta

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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 dosedependent. 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.

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