Document Detail


Development of fetal brain renin-angiotensin system and hypertension programmed in fetal origins.
MedLine Citation:
PMID:  19428956     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Since the concept of fetal origins of adult diseases was introduced in 1980s, the development of the renin-angiotensin system (RAS) in normal and abnormal patterns has attracted attention. Recent studies have shown the importance of the fetal RAS in both prenatal and postnatal development. This review focuses on the functional development of the fetal brain RAS, and ontogeny of local brain RAS components in utero. The central RAS plays an important role in the control of fetal cardiovascular responses, body fluid balance, and neuroendocrine regulation. Recent progress has been made in demonstrating that altered fetal RAS development as a consequence of environmental insults may impact on "programming" of hypertension later in life. Given that the central RAS is of equal importance to the peripheral RAS in cardiovascular regulation, studies on the fetal brain RAS development in normal and abnormal patterns could shed light on "programming" mechanisms of adult cardiovascular diseases in fetal origins.
Authors:
Caiping Mao; Lijun Shi; Feichao Xu; Lubo Zhang; Zhice Xu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2009-01-24
Journal Detail:
Title:  Progress in neurobiology     Volume:  87     ISSN:  0301-0082     ISO Abbreviation:  Prog. Neurobiol.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-05-11     Completed Date:  2009-06-16     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  0370121     Medline TA:  Prog Neurobiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  252-63     Citation Subset:  IM    
Affiliation:
Perinatal Biology Center, Soochow University School of Medicine, Suzhou 215007, China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / embryology,  physiology*
Fetal Development*
Fetus / physiopathology*
Humans
Hypertension* / etiology,  physiopathology
Renin-Angiotensin System / physiology*
Grant Support
ID/Acronym/Agency:
R01 HL089012-02/HL/NHLBI NIH HHS
Comments/Corrections

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