Source:http://linkedlifedata.com/resource/pubmed/id/11751698
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2001-12-25
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pubmed:abstractText |
Non-modulation has been suggested as a possible intermediate phenotype defining a subgroup of genetic hypertension. The trait is characterized by an attenuated response of renal blood flow and/or aldosterone to angiotensin (Ang) II. We tested the hypothesis that functional polymorphisms of the core promoter of the angiotensinogen gene are associated with non-modulation. Fifty-six young, white, male, untreated hypertensive patients and 65 age-matched normotensive volunteers were genotyped for 3 known functional variants of the angiotensinogen core promoter. All subjects were infused with 2 doses (0.5 and 3 ng/kg per minute) of Ang II while they were on a high sodium diet (250 mmol/d). The blood pressure, renal plasma flow, and aldosterone responses to Ang II were not affected by the -6 G/A polymorphism. The -20 A/C variant had no significant effects on the blood pressure or renal hemodynamic response to Ang II. However, the aldosterone response to both doses of Ang II was significantly decreased in -20 C allele carriers compared with -20 AA homozygotes in a multivariate analysis. The -18 T allele was not detected in our population, and there was a linkage dysequilibrium between -20 C and -6 A: -20 C almost exclusively occurred on the -6 A allele. Haplotype analysis indicated that the -20 C/-6 A haplotype but not the -20 A/-6 A haplotype was associated with a decreased aldosterone response to Ang II. We conclude that the -20 C variant or the -20 C/-6 A haplotype of the angiotensinogen core promoter is associated with a blunted aldosterone response to Ang II and may thus contribute to the non-modulating phenotype.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1524-4563
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1250-4
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11751698-Adult,
pubmed-meshheading:11751698-Aldosterone,
pubmed-meshheading:11751698-Angiotensinogen,
pubmed-meshheading:11751698-Angiotensins,
pubmed-meshheading:11751698-Genetic Linkage,
pubmed-meshheading:11751698-Genotype,
pubmed-meshheading:11751698-Humans,
pubmed-meshheading:11751698-Hypertension,
pubmed-meshheading:11751698-Male,
pubmed-meshheading:11751698-Promoter Regions, Genetic,
pubmed-meshheading:11751698-Sodium, Dietary,
pubmed-meshheading:11751698-Transcription, Genetic
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pubmed:year |
2001
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pubmed:articleTitle |
Angiotensinogen gene core promoter variants and non-modulating hypertension.
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pubmed:affiliation |
Department of Medicine/Nephrology, University of Erlangen-Nürnberg, Nürnberg, Germany.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Controlled Clinical Trial,
Research Support, Non-U.S. Gov't
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