Document Detail


Endothelial dysfunction. An important mediator in the pathophysiology of hypertension during pre-eclampsia.
MedLine Citation:
PMID:  22728575     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pre-eclampsia is defined as new onset hypertension with proteinuria during pregnancy. It affects approximately 5% of pregnancies in the US with a subset of those progressing into more severe forms of the disease, known as HELLP or eclampsia. Pre-eclampsia is associated with intrauterine growth restriction, chronic immune activation and multi-organ endothelial dysfunction thus contributing to the clinically visible elevation in maternal blood pressure. The end result is increased infant and maternal morbidity and mortality thereby contributing to the gross health care expenditure nationwide. Although the underlying cause of this disease is still unknown, the most well accepted hypothesis is that placental ischemia/hypoxia results from inadequate uteroplacental vascular remodeling, which leads to a decrease in placental blood flow. The ischemic placenta releases factors such as the soluble VEGF receptor-1 (sFlt-1), the angiotensin II type-1 receptor autoantibody (AT1-AA), and cytokines such as TNF-α and Interleukin 6 which cause maternal endothelial dysfunction characterized by elevated circulating endothelin (ET-1), reactive oxygen species (ROS), and enhanced vascular sensitivity to angiotensinII. These factors act in concert to decrease renal function and cause hypertension during pregnancy. Understanding the link between placental ischemia, endothelial dysfunction and hypertension during pregnancy will lend to better prediction, prevention and treatment strategies for women and children stricken by this devastating disease.
Authors:
B Lamarca
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Minerva ginecologica     Volume:  64     ISSN:  0026-4784     ISO Abbreviation:  Minerva Ginecol     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-06-25     Completed Date:  2012-12-03     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  0400731     Medline TA:  Minerva Ginecol     Country:  Italy    
Other Details:
Languages:  eng     Pagination:  309-20     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, MS, USA. bblamarca@umc.edu
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MeSH Terms
Descriptor/Qualifier:
Anoxia / physiopathology
Brain / physiopathology
Endothelium, Vascular / physiopathology*
Female
Humans
Hypertension, Pregnancy-Induced / physiopathology*
Liver / physiopathology
Pre-Eclampsia / physiopathology*
Pregnancy
Grant Support
ID/Acronym/Agency:
F32 HL078147/HL/NHLBI NIH HHS; HD65741/HD/NICHD NIH HHS; HL51971/HL/NHLBI NIH HHS; HL78147/HL/NHLBI NIH HHS; P01 HL051971/HL/NHLBI NIH HHS; R01 HD067541/HD/NICHD NIH HHS
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