Document Detail


Renin angiotensin signaling in normal pregnancy and preeclampsia.
MedLine Citation:
PMID:  21266264     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Many reports indicate that there is an increase in almost all of the components of the renin-angiotensin system (RAS) during an uncomplicated pregnancy, but renin activity, angiotensin II, and aldosterone decrease in preeclampsia (PE) for reasons that are unclear. PE is a life-threatening disorder of late pregnancy characterized by hypertension, proteinuria, increased soluble fms-like tyrosine kinase-1, as well as renal and placental morphologic abnormalities. Although a leading cause of maternal and perinatal morbidity and mortality, the pathogenic mechanisms of PE remain largely undefined. Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder. Bridging these two concepts, numerous studies report the presence of the angiotensin II type I receptor agonistic autoantibody (AT(1)-AA) found circulating in preeclamptic women. This autoantibody induces many key features of the disorder through AT(1) receptor signaling, and has been implicated in the pathogenesis of PE. Here we review the functions of the RAS during normal pregnancy and PE, and highlight the role of AT(1)-AA in both animal models and in the human disorder.
Authors:
Roxanna A Irani; Yang Xia
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Seminars in nephrology     Volume:  31     ISSN:  1558-4488     ISO Abbreviation:  Semin. Nephrol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-26     Completed Date:  2011-06-08     Revised Date:  2012-02-10    
Medline Journal Info:
Nlm Unique ID:  8110298     Medline TA:  Semin Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  47-58     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Department of Biochemistry & Molecular Biology, University of Texas at Houston Medical School, 6431 Fannin Street, Houston, TX 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism,  physiology*
Animals
Autoantibodies / metabolism
Female
Humans
Models, Animal
Pre-Eclampsia / physiopathology*
Pregnancy / metabolism,  physiology*
Receptor, Angiotensin, Type 1 / metabolism,  physiology
Renin-Angiotensin System / physiology*
Signal Transduction / physiology*
Grant Support
ID/Acronym/Agency:
R01 HL076558-01A1/HL/NHLBI NIH HHS; R01 HL076558-02/HL/NHLBI NIH HHS; R01 HL076558-03/HL/NHLBI NIH HHS; R01 HL076558-04/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Autoantibodies; 0/Receptor, Angiotensin, Type 1; 11128-99-7/Angiotensin II

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