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Blood pressure and metabolic phenotypes in relation to the ADRB1 Arg389Gly and ADRA2B I/D polymorphisms in a White population

Journal of Human Hypertension volume 22, pages 864–867 (2008)Cite this article

Previous studies of cases and controls or selected patients demonstrated association of the ADRB1 Arg389Gly and ADRA2B I/D polymorphisms with blood pressure, measures of obesity, and/or serum lipids. In multivariate-adjusted analyses of 1881 subjects randomly recruited from a White population, ADRB1 ArgArg homozygotes, compared with Gly allele carriers, had higher diastolic blood pressure (79.4 vs 78.4 mm Hg; P =0.012), and higher serum high-density lipoprotein (HDL) cholesterol (1.33 vs 1.29 mmol l−1; P =0.020), whereas none of the other cardiovascular or metabolic phenotypes reached significance in relation to the two polymorphisms. Our family-based design excluded population stratification as a possible explanation for the significant association of the ADRB1 Arg389Gly polymorphism with blood pressure and HDL cholesterol.

The β1 (ADRB1) and α2B (ADRAB2) adrenergic receptors are important in the regulation of blood pressure (BP), cardiovascular function and lipid metabolism. Their genes locate to chromosomes 10q24–26 and 2p13–q13, respectively. The ADRB1 Arg389Gly polymorphism leads to the substitution of the amino acid arginine by glycine near to the intracellular carboxyl terminal, which is involved in G-protein binding.1 The ADRA2B insertion/deletion (Ins+910Del (I/D)) polymorphism involves the deletion of three glutamic acids from a repeat element in the third intracellular loop of the protein.2 ADRB1 Arg allele carriers have increased adenyl cyclase activity in response to agonists, such as isoproterenol, epinephrine and norepinephrine.1 The ADRA2B deletion results in a loss of agonist-promoted desensitization.3

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Acknowledgements

The Flemish Study on Environment, Genes and Health Outcomes (FLEMENGHO) is a part of the European Project on Genes in Hypertension (EPOGH), which is endorsed by the European Council for Cardiovascular Research and the European Society of Hypertension. Research included in the present study was partially funded by the European Union (Grants IC15-CT98-0329-EPOGH, LSHM-CT-2006-037093 InGenious HyperCare, and HEALTH-F4-2007-201550 HyperGenes), the Fonds voor Wetenschappelijk Onderzoek Vlaanderen, Brussels, Belgium (Grants G.0256.05 and G.0575.06), the Katholieke Universiteit Leuven, Leuven, Belgium (Grants OT/04/34 and OT/05/49), the Else Kröner-Fresenius foundation (P27/05//A24/05//F01), the Heisenberg professorship (Eva Brand) from the Deutsche Forschungsgemeinschaft (Br1589/8-1) and the German Ministry for Education and Science (BMBF 0313040C), Berlin, Germany.

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Authors and Affiliations

  1. Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy

    V Tikhonoff & E Casiglia

  2. Department of Cardiovascular Diseases, Division of Hypertension and Cardiovascular Rehabilitation, Studies Coordinating Centre, University of Leuven, Leuven, Belgium

    V Tikhonoff, T Kuznetsova, L Thijs, Y Jin, T Richart & J A Staessen

  3. Department of Internal Medicine D, Nephrology and Hypertension, University Clinic of Muenster, Muenster, Germany

    S Hasenkamp & E Brand

  4. Institute of Internal Medicine, Novosibirsk, Russia

    T Kuznetsova

  5. Department of Epidemiology, University of Maastricht, Maastricht, The Netherlands

    T Richart & J A Staessen

  6. Department of Cardiology, The First Affiliated Hospital, Nanjing Medical University, Nanjing, China

    H Zhang

  7. Department of Molecular Genetics of Cardiovascular Disease, Leibniz-Institute for Arteriosclerosis Research, University of Muenster, Muenster, Germany

    S-M Brand-Herrmann

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Correspondence to V Tikhonoff.

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None of the authors has a conflict of interest with regard to the data presented in this paper.

Supplementary Information accompanies the paper on the Journal of Human Hypertension website (http://www.nature.com/jhh)

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Tikhonoff, V., Hasenkamp, S., Kuznetsova, T. et al. Blood pressure and metabolic phenotypes in relation to the ADRB1 Arg389Gly and ADRA2B I/D polymorphisms in a White population. J Hum Hypertens 22, 864–867 (2008). https://doi.org/10.1038/jhh.2008.73

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