Preeclampsia: An imbalance in placental prostacyclin and thromboxane Production

Walsh, Scott W.

doi:10.1016/s0002-9378(85)80223-4

Cited by 580 publications

(191 citation statements)

References 8 publications

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“…In PE women, TXA2 production is significantly increased while PGI2 and PGE2 production are significantly decreased and results in vasoconstriction [17]. It has been reported that placental trophoblast cells are the major source of TX production in placental tissue and that trophoblast cells from PE placentas produce significantly more TX than normal placentas [8,17], although the possibility exists that vasoconstrictors may or may not exert their actions through TXA receptor [20,38].…”

Section: Discussionmentioning

confidence: 99%

“…It has been demonstrated that multiple mechanisms contribute to the increased vascular resistance during PE, including increased vascular sensitivity to angiotensin II (ANG II) [4,5], the presence of angiotensin II receptor-1 (AT 1 ) autoantibody [2,6], an imbalance between the vasoconstrictor thromboxane (TX) and decreased vasodilator prostacyclin (PGI2) [7,8], and altered endothelin (ET) [9,10] and nitric oxide (NO) [11] levels in both the maternal circulation and in the placenta in women with PE. These alterations may result in a detrimental positive feedback system that promotes inflammation and further vasoconstriction.…”

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: Introductionmentioning

confidence: 99%

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

2007

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“…The use of PE-CM is based on several previous published studies showing that preeclamptic placental tissues produce more vasoactivators such as thromboxane and Ang II [2,4,6,17]. Placental VSMCs/ collagen gels were incubated with serum free DMEM as a control.…”

Section: Collagen Gel Contraction-induced By Native Vasoconstrictors mentioning

confidence: 99%

“…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%

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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“…As shown by early studies (5,9), trophoblasts are a major source of TX as compared to its counter partner PGI2 produced by the placenta. In vitro studies have demonstrated trophoblasts from preeclamptic placentas produced more TX than trophoblasts from normal placentas (9,10). The imbalance of increased TX production and reduced PGI2 production by preeclamptic trophoblasts is believed to contribute to the increased vasoconstriction in preeclampsia.…”

Section: Introductionmentioning

confidence: 99%

Predominant Basal Directional Release of Thromboxane, but not Prostacyclin, by Placental Trophoblasts from Normal and Preeclamptic Pregnancies

Zhao

Lewis

et al. 2008

Placenta

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Objective-To investigate apical and basal releases of thromboxane (TX) and prostacyclin (PGI2) by trophoblasts (TCs) from normal and preeclamptic (PE) placentas.Methods-TCs isolated from normal and PE placentas were incubated in cell culture inserts for 48hrs. Medium from the upper (apical) and the lower (basal) chambers were then collected separately and measured for TX and PGI2 by their stable metabolites of TXB2 and 6-keto PGF1α by ELISA. Apical and basal releases of TX and PGI were also examined with apical exposure of TCs to arachidonic acid (AA)+/-aspirin at different concentrations. Villous tissue expressions for PGI synthase, TX synthase and TX (TP) receptor were examined by immunohistochemistry.Results-1) TXB2, but not 6-keto PGF1α, concentrations were significantly higher in the lower than in the upper chambers with both normal and PE TCs (p<0.01); 2) apical exposure of TCs to AA resulted in a significant increase in TX releases towards both the upper and the lower chambers in normal TCs (p<0.01), but only a significant increase in the upper chamber in PE TCs (p < 0.01); 3) aspirin could attenuate AA-induced TX release both in the upper and the lower chambers in normal, but not in PE, TCs (p<0.01), respectively; 4) there were no differences in 6-keto PGF1α productions both in normal and PE TCs treated with AA +/− aspirin; 5) intense staining of TX synthase and TP receptor was seen in syncytiotrophoblast layer, villous core vessels and stromal cells in preeclamptic placental tissue sections.Conclusion-Predominant basal release of TX together with intense staining of TX synthase and TP receptor in trophoblasts, stromal cells and villous core vessels are found in placentas from PE. We speculate if predominant basal release of TX by TCs occurs in vivo as we found in our in vitro culture condition, basal released TX may play a significant role in increased placental vasoconstriction such as in PE.

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Preeclampsia: An imbalance in placental prostacyclin and thromboxane Production

Cited by 580 publications

References 8 publications

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

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

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

Predominant Basal Directional Release of Thromboxane, but not Prostacyclin, by Placental Trophoblasts from Normal and Preeclamptic Pregnancies

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