gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Salt intake modulates the genetic association between left ventricular mass and AGTR2 G1675A and ACE I/D

Modulation der genetischen Assoziation zwischen linksventrikulärer Masse und AGTR2 G1675A sowie ACE I/D durch Salzkonsum

Meeting Abstract

  • E. Brand - Universitätsklinikum Münster (Münster, D)
  • T. Kuznetsova - University of Leuven, Leuven
  • J.A. Staessen - University of Leuven, Leuven
  • G. Bianchi - University of Leuven, Leuven
  • E. Casiglia - University of Leuven, Leuven
  • R. Fargard - University of Leuven, Leuven
  • S.M. Brand-Herrmann - University of Leuven, Leuven
  • S.M. Brand-Herrmann - Universitätsklinikum Münster (Münster, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP130

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/hoch2005/05hoch130.shtml

Published: August 8, 2006

© 2006 Brand et al.
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Outline

Text

c-In the European Project On Genes in Hypertension (EPOGH), we investigated in 3 populations to what extent left ventricular mass (LVM) was associated with genetic variation in the angiotensin II receptors type 1 (AGTR1 A1166C) and type 2 (AGTR2 G1675A) while accounting for possible gene-gene interactions with the angiotensin-converting enzyme (ACE I/D) and angiotensinogen (AGT -532C/T) polymorphisms.

Methods and Results-We randomly recruited 221 nuclear families (384 parents, 431 offspring) in Cracow (Poland), Novosibirsk (Russia), and Mirano (Italy). Echocardiographic LVM was indexed to body surface area, adjusted for covariates, and subjected to multivariate analyses using generalized estimating equations and quantitative transmission disequilibrium tests in a population-based and family-based approach, respectively. For AGTR1 and AGTR2, there was

no heterogeneity in the phenotype-genotype relations across populations. LVM index was unrelated to the AGTR1 A1166C polymorphism. In men, in the population- and family-based analyses, the allelic effects of the AGTR2 polymorphism on LVM index differed (P=0.01) according to sodium excretion. In women, this gene-environment interaction did not reach statistical significance. In untreated men, LVM index (4.2 g/m2 per 100 mmol) and left

ventricular internal diameter (0.73 mm/100 mmol) increased (P<0.02) with higher sodium excretion in the presence of the G allele with an opposite tendency in A allele carriers. The ACE I/D polymorphism, together with the ACE genotype-by-sodium interaction term, significantly and independently improved the models relating LVM index to the AGTR2 polymorphism and the AGTR2 genotype-by-sodium interaction.

Conclusions-The present findings support the hypothesis that in men the AGTR2 G1675A and the ACE I/D polymorphisms independently influence LVM and that salt intake modulates these genetic effects.