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Regulation of fetoplacental vascular bed by hypoxia
V. Hampl, V. Jakoubek
Language English Country Czech Republic
Document type Review
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- MeSH
- Acute Disease MeSH
- Vascular Resistance MeSH
- Chronic Disease MeSH
- Financing, Organized MeSH
- Hemodynamics MeSH
- Fetal Hypoxia complications metabolism physiopathology MeSH
- Ion Channels metabolism MeSH
- Humans MeSH
- Placental Circulation MeSH
- Fetal Growth Retardation etiology physiopathology MeSH
- Signal Transduction MeSH
- Muscle, Smooth, Vascular metabolism physiopathology MeSH
- Pregnancy MeSH
- Vasoconstriction MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Review MeSH
Important fetal and perinatal pathologies, especially intrauterine growth restriction (IUGR), are thought to stem from placental hypoxia-induced vasoconstriction of the fetoplacental vessels, leading to placental hypoperfusion and thus fetal undernutrition. However, the effects of hypoxia on the fetoplacental vessels have been surprisingly little studied. We review here available experimental data on acute hypoxic fetoplacental vasoconstriction (HFPV) and on chronic hypoxic elevation of fetoplacental vascular resistance. The mechanism of HFPV includes hypoxic inhibition of potassium channels in the plasma membrane of fetoplacental vascular smooth muscle and consequent membrane depolarization that activates voltage gated calcium channels. This in turn causes calcium influx and contractile apparatus activation. The mechanism of chronic hypoxic elevation of fetoplacental vascular resistance is virtually unknown except of signs of the involvement of morphological remodeling.
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Lit.: 49
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- $a Important fetal and perinatal pathologies, especially intrauterine growth restriction (IUGR), are thought to stem from placental hypoxia-induced vasoconstriction of the fetoplacental vessels, leading to placental hypoperfusion and thus fetal undernutrition. However, the effects of hypoxia on the fetoplacental vessels have been surprisingly little studied. We review here available experimental data on acute hypoxic fetoplacental vasoconstriction (HFPV) and on chronic hypoxic elevation of fetoplacental vascular resistance. The mechanism of HFPV includes hypoxic inhibition of potassium channels in the plasma membrane of fetoplacental vascular smooth muscle and consequent membrane depolarization that activates voltage gated calcium channels. This in turn causes calcium influx and contractile apparatus activation. The mechanism of chronic hypoxic elevation of fetoplacental vascular resistance is virtually unknown except of signs of the involvement of morphological remodeling.
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