Expression of AT4R was increased in term placentae, with a significant reduction in PE placentae. Moreover, culture with AngIV or AngII increased EVT invasion from placental explants, which showed increased trophoblast proliferation and reduced apoptosis.
So the expression of the placental gene that makes a receptor for angiotensin -- receptors pull ang out of the bloodstream and keep it from raising blood pressure etc. -- is reduced in preeclamptics. For whatever reason, the placenta's turned that off, probably because it wants to raise our blood pressure to pump more blood across the shallow interface.
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