The control of blood flow to the placenta

Poston, Lucilla

doi:10.1113/expphysiol.1997.sp004033

Cited by 88 publications

(44 citation statements)

References 34 publications

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“…These models of compromised pregnancy include overfed adolescents, underfed adolescents and adults, as well as environmental heat-stress, hypoxic stress, and multiple fetuses. These observations agree with those in women, in which placental perfusion is reduced in pregnancies with growth restricted fetuses (Poston, 1997;Moore et al, 2004;Redmer et al, 2004;Huppertz and Peeters, 2005).…”

Section: Further Evidence For the Importance Of Placental Angiogenesisupporting

confidence: 82%

Uteroplacental vascular development and placental function: an update

Reynolds¹,

Borowicz²,

Caton³

et al. 2010

Int. J. Dev. Biol.

159

113

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The importance of the placenta and its vascular development to fetal growth and development has been appreciated since ancient times. Based on numerous studies in humans and animal model organisms in the last 2-3 decades, normal placental angiogenesis is critically important to ensure adequate blood flow to the placenta and therefore to provide the substrates that support normal fetal growth. Placental angiogenesis is abnormal at term in compromised pregnancies (those in which fetal growth is altered), including those resulting from maternal nutritional or environmental stress, maternal age, increased numbers of fetuses, maternal or fetal genotype, or the use of assisted reproductive technologies (e.g., cloning by somatic cell nuclear transfer). We and others have recently shown that these defects in placental vascular development occur quite early in pregnancy and may therefore presage compromised fetal growth and development. The challenges will be to find biomarkers of abnormal placental angiogenesis and to develop therapeutic strategies to "rescue" placental vascular development and thus fetal growth in compromised pregnancies. Animal models will be essential in meeting these challenges.

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Section: Further Evidence For the Importance Of Placental Angiogenesisupporting

confidence: 82%

Uteroplacental vascular development and placental function: an update

Reynolds¹,

Borowicz²,

Caton³

et al. 2010

Int. J. Dev. Biol.

159

113

View full text Add to dashboard Cite

show abstract

“…The stem villous artery was chosen because it is the major site of resistance in the placenta; the umbilical and chorionic plate vessels do not contribute greatly to vascular resistance. 27 The isolated arteries were then cut into rings and mounted on a wire myograph system. 28 The arteries were bathed in HEPES-PSS at 37°C and at pH 7.4 for 30 minutes before any manipulation and throughout the duration of the experiment.…”

Section: Tissue Preparationmentioning

confidence: 99%

Effect of Adrenomedullin on Placental Arteries in Normal and Preeclamptic Pregnancies

et al. 2001

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Abstract-Adrenomedullin is a potent vasodilatory peptide with plasma levels that increase during pregnancy. Although fetoplacental adrenomedullin levels are reported to increase in preeclampsia, maternal plasma levels may be elevated or decreased, or they may resemble those in normal pregnancy. In other hypertensive conditions, adrenomedullin increases. Therefore, we hypothesized that maternal plasma adrenomedullin levels would be higher in hypertensive pregnancies than in normotensive pregnancies and that the higher placental resistance found in preeclamptic pregnancies results from blunted activity of adrenomedullin on the vasculature. Adrenomedullin concentrations in plasma from women with normotensive pregnancies, gestational hypertension, and preeclampsia were determined by radioimmunoassay. Stem villous arteries from normotensive and preeclamptic pregnancies were dissected and mounted on a wire myograph system. Arteries were first preconstricted to 80% of their maximum constriction with U46619, a thromboxane A 2 mimetic, and exposed to cumulative doses of adrenomedullin (1ϫ10 Ϫ9 to 3ϫ10 Ϫ7 mol/L). Contrary to our hypothesis, there were no significant differences in maternal plasma adrenomedullin levels among patients with normal pregnancies, gestational hypertension, and preeclampsia. Adrenomedullin significantly relaxed arteries from both normal and preeclamptic placentas, but there was no significant difference between the 2 groups. During normal pregnancy, adrenomedullin may contribute to the low placental vascular resistance. This pathway appears to be intact in preeclampsia. We conclude that the increased placental vascular resistance observed in preeclampsia is due neither to reduced adrenomedullin secretion nor to an attenuated vascular responsiveness. Moreover, unlike other hypertensive disorders, there is no compensatory rise in circulating adrenomedullin levels. (Hypertension. 2001;37:227-231.)

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“…Indeed, all components of the RAS have been detected in the placenta, and the intra-placental RAS has been proposed to play an important role in regulating utero-placental blood flow. [13][14][15] Further to this, studies with AT1a-deficient mice demonstrate that this receptor is essential for normal placental functioning. 16 To our knowledge, few comprehensive quantitative ontogenic studies of change in placental Ang II receptor expression have been performed.…”

Section: Figurementioning

confidence: 99%

The midgestational maternal blood pressure decline is absent in mice lacking expression of the angiotensin II AT2 receptor

Carey

Rose

2010

J Renin Angiotensin Aldosterone Syst

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The midgestational maternal blood pressure (BP) decrease is absent in mice treated with an angiotensin II AT2 receptor blocker. We tested the hypotheses that there would be 1) no midgestational decrease in maternal systolic BP (SBP) in AT2-/-mice, and 2) a pattern of increased AT2 and/or decreased AT1a mRNA expression in tissues from normal (wild-type, WT) mice, corresponding with SBP changes. Heart, aorta, placenta and kidney tissue were obtained from WT and AT2-/-mice before pregnancy and on gestational days (Gd) 5-6, 12-13 and 18-19. AT1a and AT2 mRNA expression was quantified. SBP was measured. SBP was significantly decreased in WT Gd12-13 mice, but did not change during pregnancy in AT2-/-mice. In WT mice, aortic AT1a mRNA expression levels were significantly higher at Gd12-13 and Gd18-19 compared with before pregnancy. AT1a kidney and heart mRNA did not change during pregnancy. There were no changes in AT2 mRNA expression. There was no distinct pattern of change in AT1a expression in AT2-/-mice. Placental AT1a and AT2 expression levels increased markedly between Gd12-13 and Gd18-19 in WT mice. We conclude that the AT2 receptor is essential for the midgestational SBP decline in WT mice. There is no consistent relationship between changes in tissue angiotensin II receptor mRNA expression and SBP in WT mice.

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The control of blood flow to the placenta

Cited by 88 publications

References 34 publications

Uteroplacental vascular development and placental function: an update

Uteroplacental vascular development and placental function: an update

Effect of Adrenomedullin on Placental Arteries in Normal and Preeclamptic Pregnancies

The midgestational maternal blood pressure decline is absent in mice lacking expression of the angiotensin II AT2 receptor

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