Document Detail

Prenatal dehydration alters renin-angiotensin system associated with angiotensin-increased blood pressure in young offspring.
MedLine Citation:
PMID:  19779489     Owner:  NLM     Status:  MEDLINE    
The renin-angiotensin system (RAS) has an important role in cardiovascular homeostasis. This study determined the influence of water deprivation during pregnancy on the development of the RAS in rats, and examined blood pressure (BP) in the adolescent offspring. Pregnant rats were water deprived for 3 days at late gestation, and we examined fetal cardiac ultrastructure, as well as heart angiotensin (Ang) II receptor protein and mRNA, liver angiotensinogen and plasma Ang II concentrations. We also tested cardiovascular responses to i.v. Ang II in the young offspring. In utero exposure to maternal water deprivation significantly decreased fetal body and heart weight, and increased fetal plasma sodium and osmolality. Fetal liver angiotensinogen mRNA, plasma Ang I and Ang II concentrations were also increased. Although fetal AT(1a) and AT(1b) receptor mRNA and AT(1) protein were not changed, AT(2) receptor mRNA and protein levels in the heart were significantly increased following maternal dehydration. Prenatal exposure to maternal water deprivation had no effect on baseline BP; however, it significantly increased BP in response to i.v. Ang II infusion, and decreased baroreflex sensitivity in the offspring. In addition, the heart AT(2) receptor mRNA and protein were higher in the offspring exposed to prenatal dehydration. The results of this study demonstrate that prenatal dehydration affected the RAS development associated with an Ang II-increased BP in fetal origin.
Junchang Guan; Caiping Mao; Feichao Xu; Chunsong Geng; Liyan Zhu; Aiqing Wang; Zhice Xu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-09-25
Journal Detail:
Title:  Hypertension research : official journal of the Japanese Society of Hypertension     Volume:  32     ISSN:  1348-4214     ISO Abbreviation:  Hypertens. Res.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-03     Completed Date:  2010-02-24     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  9307690     Medline TA:  Hypertens Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  1104-11     Citation Subset:  IM    
Perinatal Biology Center, Soochow University First Affiliated Hospital, Suzhou, China.
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MeSH Terms
Angiotensin I / blood
Angiotensin II / blood
Angiotensinogen / genetics
Baroreflex / physiology
Birth Weight
Blood Pressure / physiology
Fetal Development
Gene Expression / physiology
Heart / embryology,  physiology
Heart Rate / physiology
Hypertension / physiopathology*
Liver / embryology,  physiology
Prenatal Exposure Delayed Effects / physiopathology*
RNA, Messenger / metabolism
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 / genetics,  metabolism
Receptor, Angiotensin, Type 2 / genetics,  metabolism
Renin-Angiotensin System / physiology*
Water Deprivation / physiology*
Grant Support
Reg. No./Substance:
0/RNA, Messenger; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2; 11002-13-4/Angiotensinogen; 11128-99-7/Angiotensin II; 9041-90-1/Angiotensin I
Comment In:
Hypertens Res. 2009 Dec;32(12):1051-2   [PMID:  19816502 ]

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

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