Home > Journals > Minerva Ginecologica > Past Issues > Minerva Ginecologica 2010 April;62(2) > Minerva Ginecologica 2010 April;62(2):105-20

CURRENT ISSUE
 

ARTICLE TOOLS

Reprints

MINERVA GINECOLOGICA

A Journal on Obstetrics and Gynecology


Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Scopus, Emerging Sources Citation Index


eTOC

 

  CARDIAC PROBLEMS IN PREGNANCY


Minerva Ginecologica 2010 April;62(2):105-20

language: English

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

Lamarca B.

Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS, USA


PDF  


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.

top of page

Publication History

Cite this article as

Corresponding author e-mail