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• W2407692670 endingPage "S94" @default.
• W2407692670 startingPage "S87" @default.
• W2407692670 abstract "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." @default.
• W2407692670 created "2016-06-24" @default.
• W2407692670 creator A5018439413 @default.
• W2407692670 creator A5083856804 @default.
• W2407692670 date "2009-01-01" @default.
• W2407692670 modified "2023-10-01" @default.
• W2407692670 title "Regulation of fetoplacental vascular bed by hypoxia" @default.
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• W2407692670 doi "https://doi.org/10.33549/physiolres.931922" @default.
• W2407692670 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20131940" @default.
• W2407692670 hasPublicationYear "2009" @default.
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