Format

Send to

Choose Destination
See comment in PubMed Commons below
Minerva Ginecol. 2010 Apr;62(2):105-20.

The role of immune activation in contributing to vascular dysfunction and the pathophysiology of hypertension during preeclampsia.

Author information

  • 1Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA. bblamarca@physiology.umsmed.edu

Abstract

Preeclampsia remains a leading cause of maternal death and perinatal morbidity and still the pathophysiological mechanisms of the disease remain largely unknown. The most well accepted hypothesis for the genesis of the disease is that placental ischemia/hypoxia results from inadequate remodeling of the maternal uterine spiral arteries, which leads to a decrease in uteroplacental blood flow. Subsequently factors are released from the ischemic placenta showering the maternal vascular endothelium. These factors include a host of molecules such as the soluble VEGF receptor-1 (sFlt-1), the angiotensin II type-1 receptor autoantibody (AT1-AA), and cytokines such as TNF-a and Interleukin 6 which in turn generate widespread dysfunction of the maternal vascular endothelium. This dysfunction results in elevated circulating endothelin (ET-1), reactive oxygen species (ROS), and augmented vascular sensitivity to angiotensin II as well as decreased formation of vasodilators such as nitric oxide and prostacyclin. These alterations in vascular function lead to hypertension with multi-organ dysfunction, especially in cases of early onset preeclampsia. Therefore, identifying the connection between placental ischemia and maternal cardiovascular abnormalities is an important area of investigation.

PMID:
20502423
PMCID:
PMC3740963
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Minerva Medica Icon for PubMed Central
    Loading ...
    Support Center