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  1. Judson JP, Nadarajah VD, Bong YC, Subramaniam K, Sivalingam N
    Med J Malaysia, 2006 Jun;61(2):173-80.
    PMID: 16898308
    Pre-eclampsia or pregnancy induced hypertension (PIH) affects 6-8% of all pregnancies. Although the underlying mechanism of PIH is still unknown, it is widely believed that the placenta plays an important role. It was thought that an ischemic placenta due to poor perfusion can precipitate the signs and symptoms of PIH. This study aims to investigate the possible role of Type 1(AT1) and Type 2 (AT2) angiotensin II receptor subtypes in the mechanism of PIH. AT1 receptor stimulation causes vasoconstriction and AT2 receptor stimulation causes vasodilatation. Investigating the interactions of these two receptors in the placenta provides an insight as to the balance that may exist between AT1 and AT2 receptors in normal pregnancy. Any disruption to the balance might cause a disruption of the blood flow in the placenta, leading to PIH. Placentas were collected from 11 PIH patients and 11 normal patients. Immunohistochemistry techniques were performed on the placental tissue to determine the distribution of AT1 and AT2 receptors in the placental tissue qualitatively and quantitatively. It was observed that in normal patients, the balance between AT1 and AT2 receptors is that the level of AT2 receptors is higher than the level of AT1 receptors. However in the PIH patient, it was observed that the normal balance was disrupted. In PIH patients the level of AT1 receptors was observed to be higher than the level of AT2 receptors. This study suggests that disruption of the balance between AT1 and AT2 receptors observed in PIH placentas might cause a decrease in blood flow to the placenta, causing it to be poorly perfused. This may cause placental ischemia which may lead to PIH.
    Matched MeSH terms: Pregnancy/metabolism*
  2. Singh HJ, Rahman A, Larmie ET, Nila A
    Acta Obstet Gynecol Scand, 2001 Feb;80(2):99-103.
    PMID: 11167202
    AIMS: The pathogenesis of pre-eclampsia is still unclear. Placental hypoperfusion, which precedes the maternal manifestations of pre-eclampsia, could be due to some vasoconstrictor factor/s like endothelin-1. The aim of the study therefore was to estimate the levels of endothelin-1 in feto-placental tissue homogenates from normotensive pregnant women and women with pre-eclampsia.

    METHOD AND MATERIAL: Fresh, vaginally delivered placentae from ten normotensive pregnant women and nine women with pre-eclampsia were carefully dissected and 4 gm each of amnion, chorion laeve, placental plate chorion, fetal placenta (fetal surface of the placenta) and maternal placenta (surface of the placenta attached to the uterine wall) were obtained. These tissues were then thoroughly washed in a 0.5 M phosphate buffer, pH 7.5, at room temperature and then individually homogenized for one minute in 4 ml of the same buffer. After centrifugation the supernatant was removed. The pellet was re-suspended in buffer, re-homogenized and then centrifuged. The supernatant was removed and the procedure was repeated once again and the three supernatants of each tissue were pooled. Endothelin-1 was estimated by RIA. All results are presented as mean+/-SEM. Statistical analysis was performed using students 't' test for unpaired samples and a 'p' value of <0.05 was considered significant.

    RESULTS: In tissues from normotensive pregnant women, no significant differences were evident in endothelin-1 concentrations in the chorion laeve, fetal placenta and maternal placenta but were significantly higher than those in the amnion and placental plate chorion (p<0.01). In tissues from pre-eclamptic women, no significant differences were evident between endothelin-1 concentrations in the chorion laeve, placental plate chorion and fetal placenta. Mean endothelin-1 concentration in the amnion and maternal placenta were significantly lower than those in chorion laeve, placental plate chorion and fetal placenta (p<0.01). Endothelin-1 concentrations were significantly higher in the amnion, chorion laeve, placental plate chorion and fetal placenta from women with pre-eclampsia when compared to tissues from normotensive pregnant women (p<0.01).

    CONCLUSIONS: Endothelin-1 levels were significantly higher in the placental tissues from women with pre-eclampsia. Endothelin-1, being a powerful vasoconstrictor, could cause significant vasoconstriction in the placental vasculature, and alterations in endothelin-1 levels in placental vasculature may therefore have a role in the pathogenesis of pre-eclampsia.

    Matched MeSH terms: Pregnancy/metabolism*
  3. Baharom S, De Matteo R, Ellery S, Della Gatta P, Bruce CR, Kowalski GM, et al.
    Am J Physiol Endocrinol Metab, 2017 07 01;313(1):E75-E83.
    PMID: 28325734 DOI: 10.1152/ajpendo.00450.2016
    Our aim was to determine the disposition of creatine in ovine pregnancy and whether creatine is transferred across the placenta from mother to fetus. Pregnant ewes received either1) a continuous intravenous infusion of creatine monohydrate or saline from 122 to 131 days gestation, with maternal and fetal arterial blood and amniotic fluid samples collected daily for creatine analysis and fetal tissues collected at necropsy at 133 days for analysis of creatine content, or2) a single systemic bolus injection of [13C]creatine monohydrate at 130 days of gestation, with maternal and fetal arterial blood, uterine vein blood, and amniotic fluid samples collected before and for 4 h after injection and analyzed for creatine, creatine isotopic enrichment, and guanidinoacetic acid (GAA; precursor of creatine) concentrations. Presence of the creatine transporter-1 (SLC6A8) and l-arginine:glycine amidinotransferase (AGAT; the enzyme synthesizing GAA) proteins were determined by Western blots of placental cotyledons. The 10-day creatine infusion increased maternal plasma creatine concentration three- to fourfold (P< 0.05) without significantly changing fetal arterial, amniotic fluid, fetal tissues, or placental creatine content. Maternal arterial13C enrichment was increased (P< 0.05) after bolus [13C]creatine injection without change of fetal arterial13C enrichment. SLC6A8 and AGAT proteins were identified in placental cotyledons, and GAA concentration was significantly higher in uterine vein than maternal artery plasma. Despite the presence of SLC6A8 protein in cotyledons, these results suggest that creatine is not transferred from mother to fetus in near-term sheep and that the ovine utero-placental unit releases GAA into the maternal circulation.
    Matched MeSH terms: Pregnancy/metabolism
  4. Loy SL, KNS S, JM HJ
    Prev Med, 2013;57 Suppl:S41-4.
    PMID: 23219759 DOI: 10.1016/j.ypmed.2012.11.021
    This study aimed to evaluate changes in maternal adiposity and lipid profile and to correlate these parameters with Deoxyribonucleic acid (DNA) damage and total antioxidant capacity (TAC) levels among pregnant women.
    Matched MeSH terms: Pregnancy/metabolism*
  5. Loy SL, Jan Mohamed HJ
    Women Health, 2014;54(2):145-60.
    PMID: 24329183 DOI: 10.1080/03630242.2013.870632
    This study aimed to examine the associations among prenatal nicotine exposure, oxidative stress, and postpartum visceral fat among women exposed to secondhand smoke (SHS). The study was conducted in Kelantan, Malaysia, from April 2010 to December 2012. Blood samples were collected in the second and third trimesters from 135 healthy pregnant women who were followed-up at delivery, 2 months, 6 months and 12 months postpartum. Maternal hair nicotine and oxidative stress markers during pregnancy were measured. Visceral fat was assessed by bioelectrical impedance. Multiple linear regression analysis revealed that maternal hair nicotine concentration was associated with increased DNA damage (tail moment: β=0.580, p=0.001) and decreased glutathione peroxidase (β=-12.100; p=0.009) in the second trimester of pregnancy. Increased DNA damage, protein oxidation and total antioxidant capacity in the second trimester were associated with 2, 6, and 12 months postpartum visceral fat. No direct association was found between prenatal hair nicotine level and postpartum visceral fat; however, these results suggest that any relation of SHS to visceral adiposity may be indirect, mediated via enhanced oxidative stress.
    Matched MeSH terms: Pregnancy/metabolism*
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