Document Detail

Role of the renin-angiotensin system in the pathogenesis of preeclampsia.
MedLine Citation:
PMID:  15753325     Owner:  NLM     Status:  MEDLINE    
Preeclampsia is a hypertensive disorder unique to pregnancy with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression observed both in human preeclampsia and in a transgenic mouse model with a human preeclampsia-like syndrome supports the concept that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. A novel disease paradigm of the two-kidney one-clip (2K-1C) Goldblatt model is presented for preeclampsia, wherein the gravid uterus is the clipped "kidney" and the two maternal kidneys represent the unclipped kidney. Validation of the 2K-1C Goldblatt model analogy requires evidence of elevated angiotensin II in the peripheral circulation before vascular maladaptation in preeclampsia. Convincing evidence of the elevation of angiotensin II in preeclampsia does not exist despite the fact that much of vascular pathogenesis appears to be due to angiotensin type I (AT(1)) receptor activation. Vascular maladaptation with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT(1) and bradykinin B(2) receptor heterodimerization and the production of an autoantibody against AT(1). Various organ systems with a predilection for involvement in preeclampsia are each a site of a tissue-based RAS. How angiotensin II-mediated mechanisms may explain the primary clinical-pathological features of preeclampsia is described. Future investigations are proposed to more precisely define the role of activation of the uteroplacental RAS in the mechanisms underlying preeclampsia.
Dinesh M Shah
Related Documents :
9189835 - High sensitivity test for the early diagnosis of gestational hypertension and preeclamp...
1968025 - The clinical utility of the roll-over test in predicting pregnancy-induced hypertension...
1566945 - Pregnancy-induced hypertension in north carolina, 1988 and 1989.
9715225 - Obstructive sleep apnea during pregnancy resulting in pulmonary hypertension.
2309815 - Labetalol pharmacokinetics in pregnancy-induced hypertension.
22168775 - Effects of chronic carbon monoxide exposure on fetal growth and development in mice.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  288     ISSN:  1931-857X     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2005 Apr 
Date Detail:
Created Date:  2005-03-08     Completed Date:  2005-04-18     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F614-25     Citation Subset:  IM    
Univ. of Wisconsin Medical School, Dept. of Obstetrics and Gynecology, 202 S. Park Str., Madison, WI 53715, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Pre-Eclampsia / etiology*,  physiopathology*
Renin-Angiotensin System / physiology*
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Ficoll and dextran vs. globular proteins as probes for testing glomerular permselectivity: effects o...
Next Document:  Testing the usefulness of the molecular coancestry information to assess genetic relationships in li...