Document Detail


Molecular and vascular targets in the pathogenesis and management of the hypertension associated with preeclampsia.
MedLine Citation:
PMID:  20923405     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Normal pregnancy is associated with significant hemodynamic changes and vasodilation of the uterine and systemic circulation in order to meet the metabolic demands of the mother and developing fetus. Preeclampsia (PE) is one of the foremost complications of pregnancy and a major cause of maternal and fetal mortality. The pathophysiological mechanisms of PE have been elusive, but some parts of the puzzle have begun to unravel. Genetic factors such as leptin gene polymorphism, environmental and dietary factors such as Ca(2+) and vitamin D deficiency, and co-morbidities such as obesity and diabetes may increase the susceptibility of pregnant women to develop PE. An altered maternal immune response may also play a role in the development of PE. Although the pathophysiology of PE is unclear, most studies have implicated inadequate invasion of cytotrophoblasts into the uterine artery, leading to reduced uteroplacental perfusion pressure (RUPP) and placental ischemia/hypoxia. Placental ischemia induces the release of biologically active factors such as growth factor inhibitors, anti-angiogenic factors, inflammatory cytokines, reactive oxygen species, hypoxia-inducible factors, and antibodies to vascular angiotensin II (AngII) receptor. These bioactive factors could cause vascular endotheliosis and consequent increase in vascular resistance and blood pressure, as well as glomerular endotheliosis with consequent proteinuria. The PE-associated vascular endotheliosis could be manifested as decreased vasodilator mediators such as nitric oxide, prostacyclin and hyperpolarizing factor and increased vasoconstrictor mediators such as endothelin-1, AngII and thromboxane A₂. PE could also involve enhanced mechanisms of vascular smooth muscle contraction including intracellular Ca(2+), and Ca(2+) sensitization pathways such as protein kinase C and Rho-kinase. PE-associated changes in the extracellular matrix composition and matrix metalloproteinases activity also promote vascular remodeling and further vasoconstriction in the uterine and systemic circulation. Some of these biologically active factors and vascular mediators have been proposed as biomarkers for early prediction or diagnosis of PE, and as potential targets for prevention or treatment of the disease.
Authors:
Ossama M Reslan; Raouf A Khalil
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cardiovascular & hematological agents in medicinal chemistry     Volume:  8     ISSN:  1875-6182     ISO Abbreviation:  Cardiovasc Hematol Agents Med Chem     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-06     Completed Date:  2011-02-01     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  101266881     Medline TA:  Cardiovasc Hematol Agents Med Chem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  204-26     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Female
Genomic Imprinting
Humans
Hypertension / genetics,  physiopathology*,  therapy*
Male
Mice
Pre-Eclampsia / genetics,  physiopathology*,  therapy*
Pregnancy
Rats
Risk Factors
Grant Support
ID/Acronym/Agency:
HD-60702/HD/NICHD NIH HHS; HL-65998/HL/NHLBI NIH HHS; HL-70659/HL/NHLBI NIH HHS; R01 HL065998/HL/NHLBI NIH HHS; R01 HL065998-09/HL/NHLBI NIH HHS; R01 HL070659/HL/NHLBI NIH HHS; R01 HL070659-05/HL/NHLBI NIH HHS; R03 HD060702/HD/NICHD NIH HHS; R03 HD060702-01/HD/NICHD NIH HHS; R03 HD060702-02/HD/NICHD NIH HHS
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