Document Detail


Cardiovascular consequences of genetic variation at -6/235 in human angiotensinogen using "humanized" gene-targeted mice.
MedLine Citation:
PMID:  20823378     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Genetic and functional data support a role for angiotensinogen in blood pressure control, and many population studies have suggested that polymorphisms in the angiotensinogen gene contribute to hypertension. Two common haplotypes of the human angiotensinogen gene are -6A/235T and -6G/235M. To study their contributions to blood pressure regulation in a controlled model system, we developed triple-transgenic mice expressing either -6A/235T or -6G/235M human angiotensinogen, expressing either an overexpressed and poorly regulated (REN9) or a tightly regulated (PAC160) human renin, and all carrying a null mutation in the endogenous murine angiotensinogen gene. These humanized mice were then examined for blood pressure differences at baseline and after a high-salt diet, changes in cardiovascular organ weight, and differences in angiotensinogen and renin gene expression. Mice expressing the -6G/235M haplotype on the PAC160 background exhibited increased blood pressure and cardiac hypertrophy at baseline. In contrast, all of the mice with the REN9 background had equivalent baseline blood pressures. On the REN9 background, there was a greater increase in blood pressure in -6A/235T in response to a high-salt diet, providing evidence it may be a susceptibility allele. There were no differences in angiotensinogen expression between haplotypes on either background strain. The data suggest that the impact of angiotensinogen haplotypes on cardiovascular end points may be dependent on renin status and environmental influences, such as dietary sodium. These insights may help explain the discrepancies among observational studies that have examined roles for the -6A/235T and -6G/235M angiotensinogen haplotypes in varied human populations.
Authors:
Justin L Grobe; Matthew E Dickson; Sungmi Park; Deborah R Davis; Ella J Born; Curt D Sigmund
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-09-07
Journal Detail:
Title:  Hypertension     Volume:  56     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-21     Completed Date:  2010-11-10     Revised Date:  2011-11-01    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  981-7     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
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MeSH Terms
Descriptor/Qualifier:
Alleles
Angiotensinogen / genetics*,  metabolism
Animals
Blood Pressure / genetics*
Genetic Variation
Genotype
Haplotypes
Hypertension / genetics,  metabolism
Mice
Mice, Transgenic
Renin / genetics,  metabolism
Sodium, Dietary
Telemetry
Grant Support
ID/Acronym/Agency:
DK007690/DK/NIDDK NIH HHS; HL048058/HL/NHLBI NIH HHS; HL061446/HL/NHLBI NIH HHS; HL084207/HL/NHLBI NIH HHS; HL098276/HL/NHLBI NIH HHS; K99 HL098276-01/HL/NHLBI NIH HHS; P01 HL062984-080005/HL/NHLBI NIH HHS; P01 HL062984-090005/HL/NHLBI NIH HHS; P01 HL084207-01A1/HL/NHLBI NIH HHS; P01 HL084207-01A10001/HL/NHLBI NIH HHS; P01 HL084207-02/HL/NHLBI NIH HHS; P01 HL084207-020001/HL/NHLBI NIH HHS; P01 HL084207-03/HL/NHLBI NIH HHS; P01 HL084207-030001/HL/NHLBI NIH HHS; P01 HL084207-04/HL/NHLBI NIH HHS; R01 HL061446-11/HL/NHLBI NIH HHS; R01 HL061446-12/HL/NHLBI NIH HHS; R01 HL061446-13/HL/NHLBI NIH HHS; R01 HL076421-04/HL/NHLBI NIH HHS; R37 HL048058-14/HL/NHLBI NIH HHS; R37 HL048058-15/HL/NHLBI NIH HHS; R37 HL048058-16/HL/NHLBI NIH HHS; R37 HL048058-17/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Sodium, Dietary; 11002-13-4/Angiotensinogen; EC 3.4.23.15/Renin

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