Endothelial Preeclampsia

Furthermore, high-velocity perfusion due to minimal dilatation of the terminal segments of the spiral arteries leads to hydrodynamic stress in the intervillous space. This placenta stress stimulates the release of a number of factors derived from the trophoblast, and these factors, in turn, contribute to the widespread multisystemic maternal inflammatory response observed in preeclampsia (Tjoa, Levine and Karumanchi, 2007). Such placental-derived factors comprise of the anti-angiogenic proteins, soluble Endoglin (sENG) (Venkatesha et al., 2006) and sFlT1 or soluble vascular endothelial growth factor (VEGF) receptor 1 (Maynard et al., 2003 ), as well as pro-angiogenic Placental Growth Factor (PlGF or PGF). There is elevation of sFLT1 and sENG …show more content…
In contrast, maternal preeclampsia is not necessarily linked with abnormal implantation of the placenta and reduced perfusion. Endothelial dysfunction in the maternal circulation is already present, as a result of pre-existing vascular dysfunction, this is further accentuated as a result of the physiological effects of pregnancy (Ness and Roberts 1996). The effect of poor implantation of the placenta has been incorporated into a 3-staged preeclampsia model (Redman and Sargent 2010). Incomplete tolerance induction to the allogenic fetus, which is said to occur very early in pregnancy (Stage 1), is thought to be the underlying factor that causes incomplete placentation with reduction in remodeling of spiral arteries in the maternal utero-placental circulation (Stage 2). Enhancement of endoplasmic reticulum stress and placental oxidative stress occurs, with release of different placental factors into the maternal circulation that cause endothelial dysfunction, excessive inflammation in the maternal vascular system, and subsequently the multi-systemic signs of preeclampsia (Stage 3) (Redman and Sargent