Fetal endothelin levels and placental vascular endothelin receptors in intrauterine growth retardation

McQueen, James; Kingdom, Jcp; Connell, J; Whittle, Martin

doi:10.1016/0020-7292(94)90435-9

Cited by 28 publications

(26 citation statements)

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“…ET-1 has been postulated to play a role in the patho physiology of preeclampsia [6] and intrauterine fetal growth retardation [5,11], Because there is systemic hyp oxia in many of these fetuses and because the present study suggests that hypoxia induces an increase in the plasma ET-1 concentration, ET-1 may be directly in volved in the pathogenesis of these disorders. However, there is also the possibility that plasma levels of ET-1 increase secondary to endothelial damage caused by other pathologic factors.…”

Section: Discussionmentioning

confidence: 90%

“…During pregnancy, plasma ET-1 levels in umbilical vessels are increased in pregnan cies complicated by preeclampsia [6] and intrauterine growth retardation [11]. Hypoxia is one of the stimuli that induce the production of ET-1 [2], and a relationship between fetal asphyxia and an elevation in plasma ET-1 levels in umbilical vessels has been demonstrated in human fetuses [8,9], In earlier studies, an elevation in umbilical venous plasma ET-1 concentration was related to the decrease in pH, base deficit and low Apgar score (<6) [8], and the plasma ET-1 concentration difference in the umbilical artery to vein correlates with the severity of fetal hypoxia [9], In the present study, repeated intermittent occlusion of the umbilical cord caused fetal hypoxia and/or acidemia and increased fetal plasma ET-1 levels significantly.…”

Section: Discussionmentioning

confidence: 99%

“…In earlier studies with humans, umbilical plasma ET-1 levels were found to be increased after vaginal delivery [7] and fetal asphyxia [8,9]. How ever, other studies have shown no relationship between umbilical plasma ET-1 levels and birth stress [10,11].…”

Section: Introductionmentioning

confidence: 99%

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Plasma Endothelin 1 Levels during Asphyxia in the Fetal Goat

Takada

Yoneyama

Power

et al. 1996

Gynecol Obstet Invest

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The changes in fetal carotid arterial plasma levels of endothelin-1, catecholamines, PO₂, PCO₂ and pH were measured after intermittent repetitive umbilical cord occlusion in late gestation pregnant goats (n = 9). Endothelin-1 levels increased to 3.58 ± 0.28 pg/ml immediately after the onset of fetal hypoxia, a level significantly higher than the respective values in the control period (p < 0.05). The elevation of fetal plasma endothelin-1 levels correlated inversely with carotid arterial PO₂ (r = -0.41, p < a 0.05) and pH (r = -0.43, p < 0.05). The results suggest that increased endothelin-1 levels may contribute to the maintenance of the fetal circulation during fetal asphyxia.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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Plasma Endothelin 1 Levels during Asphyxia in the Fetal Goat

Takada

Yoneyama

Power

et al. 1996

Gynecol Obstet Invest

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“…It is still uncertain as to whether increased ET-1 levels could indirectly (through the release of NO and EDHF) contribute to the decrease in vascular resistance, which normally occurs during late gestation (Greiss, 1966;Peeters et al, 1980). Nevertheless, it is likely that functional integrity of the endothelium could affect in a critical manner the vascular responses to ET-1 in both healthy and high risk pregnancies (McQueen et al, 1993). This study was supported by grants from the Mutuelle Generale de l'Education Nationale and from the Delegation a la Recherche Clinique, Assistance Publique-H6pitaux de Paris.…”

Section: Resultsmentioning

confidence: 99%

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Sabry

Mondon

Lévy

et al. 1995

British J Pharmacology

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1 The aim of this study was to assess the role of endothelial cells in the modulation of vasocontractile responses to endothelin-1 (ET-1) of human placental vasculature.2 Isolated stem villi small arteries (diameter = 170-250 gm) were obtained from healthy parturients who underwent caesarean surgery during the 39th week of pregnancy for cephalo-pelvic disproportion. Isometric tension was measured in vascular rings mounted in a myograph system and challenged with ET-1 (10-12 to 10-6 M). 3 The vasocontractile response to ET-1 was significantly (P<0.0001) increased in endothelial-denuded (active tension= 1156 + 214 mN mm-') as compared with endothelial-preserved vascular rings (active tension = 458 ± 48 mN mm-1). This difference was significantly (P< 0.05) but only partly abolished by the NO synthase inhibitor N1'-nitro-L-arginine (L-NOARG, 10' M).4 In endothelial-preserved rings submaximally precontracted with 5-hydroxytryptamine (10-6 M), ET-1 (10-12 to 10-9 M) induced dose-dependent relaxation (maximum relaxation = 70 + 7%) at 10-9 M, which was followed, at higher doses (10-8 to 10-6 M), by a contraction. In contrast, no relaxation was seen in endothelial-denuded rings. The relaxation in rings with endothelium was significantly (P<0.001) reduced by L-NOARG (10-4 M). Moreover, it was totally abolished by combined pretreatment with L-NOARG (10-4 M) and the sulphonylurea glibenclamide (10' M). 5 In conclusion, endothelial cells modulate the vascular responses to ET-1 through the release of NO and a substance acting on the ATP-sensitive K+ channel of smooth muscle of stem villi small arteries from healthy parturients.

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“…Thus, in the middle of the luteal phase (at the progesterone peak), the ET to enkephalinase ratio favours ET breakdown and therefore contributes to the absence of vasoconstriction of the implantation site vessels. Moreover, the hypothesis in which ET-1 is involved in disorders such as intrauterine growth retardation and preeclampsia seems to be confirmed by the elevated concentration of immunoreactive ET in both the umbilical vessels and the maternal blood in such cases and increased ET-1 gene expression in the placental villi in preeclampsia [28,29].…”

Section: Vasomotor Factorsmentioning

confidence: 96%

Physiopathology of human embryonic implantation: clinical incidences.

Merviel

Lourdel²,

Cabry³

et al. 2010

Folia Histochem Cytobiol.

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Embryo implantation consists of a series of events promoting the invasion of the endometrium and then the uterine arterial system by the extra-embryonic trophoblast. In order for this semi-heterologous implantation to succeed, the endometrium has to first undergo a number of structural and biochemical changes (decidualization). The decidua's various constituents subsequently play a role in the embryonic implantation. The third step is the transformation of the uterine vascular system and the growth of the placenta, which will provide the foetoplacental unit with nutrients. Several physiopathological aspects will be discussed: 1) the implantation window, regulated by maternal and embryonic hormonal secretions and thus influenced by any defects in the latter: dysharmonic luteal phase, 21-hydroxylase block, abnormal integrin expression, 2) the successive trophoblast invasions of uterine vessels which, when defective, lead to early embryo loss or late-onset vascular pathologies, as preeclampsia, 3) the pregnancy's immunological equilibrium, with a spontaneously tolerated semi-allogeneic implant, 4) the impact of pro-coagulant factors (thrombophilia) on the pregnancy's progression, 5) the environment of the uterus, ranging from hydrosalpinx to uterine contractions. In summary, the least anatomical or physiological perturbation can interfere with human embryonic implantation -a very particular phenomenon and a true biological paradox.

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Fetal endothelin levels and placental vascular endothelin receptors in intrauterine growth retardation

Cited by 28 publications

References 0 publications

Plasma Endothelin 1 Levels during Asphyxia in the Fetal Goat

Plasma Endothelin 1 Levels during Asphyxia in the Fetal Goat

Endothelial modulation of vasoconstrictor responses to endothelin‐1 in human placental stem villi small arteries

Physiopathology of human embryonic implantation: clinical incidences.

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