Document Detail


Angiotensin II type 2 receptor is essential for left ventricular hypertrophy and cardiac fibrosis in chronic angiotensin II-induced hypertension.
MedLine Citation:
PMID:  11457756     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The roles of angiotensin II (Ang II) in the regulation of heart function under normal and pathological conditions have been well documented. Although 2 types of Ang II receptor (AT(1) and AT(2)) are found in various proportions, most studies have focused on AT(1)-coupled events. In the present study, we examined the hypothesis that signaling by AT(2) is important to the development of left ventricular hypertrophy and cardiac fibrosis by Ang II infusion in mice lacking the AT(2) gene (Agtr2-/Y). METHODS AND RESULTS: Male Agtr2-/Y and age-matched wild-type (WT) mice were treated long-term with Ang II, infused at a rate of 4.2 ng. kg(-1). min(-1) for 3 weeks. Ang II elevated systolic blood pressure to comparable levels in Agtr2-/Y and WT mice. WT mice developed prominent concentric cardiac hypertrophy, prominent fibrosis, and impaired diastolic relaxation after Ang II infusion. In contrast, there was no cardiac hypertrophy in Agtr2-/Y mice. Agtr2-/Y mice, however, did not show signs of heart failure or impairment of ventricular relaxation and only negligible fibrosis after Ang II infusion. The absence of fibrosis may be a clue to the absence of impairment in ventricular relaxation and account for the normal left ventricular systolic and diastolic performances in Agtr2-/Y mice. CONCLUSIONS: Chronic loss of AT(2) by gene targeting abolished left ventricular hypertrophy and cardiac fibrosis in mice with Ang II-induced hypertension.
Authors:
S Ichihara; T Senbonmatsu; E Price; T Ichiki; F A Gaffney; T Inagami
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  104     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2001 Jul 
Date Detail:
Created Date:  2001-07-17     Completed Date:  2001-08-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  346-51     Citation Subset:  AIM; IM    
Affiliation:
Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II*
Animals
Chronic Disease
Collagen / biosynthesis,  genetics
Diastole
Disease Models, Animal
Echocardiography
Echocardiography, Doppler
Endomyocardial Fibrosis / complications,  etiology*,  pathology
Fibronectins / biosynthesis,  genetics
Hypertension / chemically induced,  complications,  metabolism*,  pathology
Hypertrophy, Left Ventricular / complications,  etiology*,  pathology
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardium / metabolism,  pathology
RNA, Messenger / biosynthesis
Receptor, Angiotensin, Type 1
Receptor, Angiotensin, Type 2
Receptors, Angiotensin / biosynthesis,  deficiency*,  genetics,  metabolism
Systole
Transforming Growth Factor beta / biosynthesis,  genetics
Transforming Growth Factor beta1
Grant Support
ID/Acronym/Agency:
DK-20593/DK/NIDDK NIH HHS; HL-58205/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Fibronectins; 0/RNA, Messenger; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2; 0/Receptors, Angiotensin; 0/Tgfb1 protein, mouse; 0/Transforming Growth Factor beta; 0/Transforming Growth Factor beta1; 11128-99-7/Angiotensin II; 9007-34-5/Collagen
Comments/Corrections
Comment In:
Circulation. 2001 Jul 17;104(3):247-8   [PMID:  11457738 ]

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