Regulation of fetoplacental vascular bed by hypoxia.
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.
Center for Cardiovascular Research, Prague, Czech Republic. vaclav.hampl@lf2.cuni.cz
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Hampl
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Jakoubek
D000208:Acute Disease; D000818:Animals; D002908:Chronic Disease; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000503:physiopathology; D005311:Fetal Hypoxia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000503:physiopathology; D021041:Placental Circulation; D011247:Pregnancy; D015398:Signal Transduction; D014655:Vascular Resistance; D014661:Vasoconstriction
D007473:Ion Channels