| Renin angiotensin signaling in normal pregnancy and preeclampsia. | |
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MedLine Citation:
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PMID: 21266264 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Roxanna A Irani; Yang Xia |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Seminars in nephrology Volume: 31 ISSN: 1558-4488 ISO Abbreviation: Semin. Nephrol. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-26 Completed Date: 2011-06-08 Revised Date: 2012-02-10 |
Medline Journal Info:
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Nlm Unique ID: 8110298 Medline TA: Semin Nephrol Country: United States |
Other Details:
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Languages: eng Pagination: 47-58 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Biochemistry & Molecular Biology, University of Texas at Houston Medical School, 6431 Fannin Street, Houston, TX 77030, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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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:
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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:
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0/Autoantibodies; 0/Receptor, Angiotensin, Type 1; 11128-99-7/Angiotensin II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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