The BK (bradykinin) B2 receptor is the major cellular mediator of the effects of BK. A 9 bp deletion in the promoter of the receptor gene represents an allelic variant that is associated with enhanced mRNA expression levels. We tested whether this polymorphism is associated with the prevalence of MI (myocardial infarction) or with echocardiographically determined left ventricular function in post-MI patients. Patients with documented MI (n=484), matched controls and controls without evidence of coronary heart disease (n=1363) constituted cases and controls. MI patients and controls were carefully matched for age, gender and cardiovascular risk factors. Genotype distributions of the 9 bp insertion/deletion polymorphism were similar across the groups: −9/−9, −9/+9 and +9/+9 were 22.1, 49.5 and 28.5% in MI patients, and 23.0, 44.6 and 32.5% in matched control subjects respectively. The lack of association was also observed in selected subgroups, stratified by age, gender and cardiovascular risk factors. Furthermore, there was no relation between this polymorphism and left ventricular systolic function in post-MI patients. These findings indicate that the 9 bp insertion/deletion polymorphism of the BK B2 receptor gene is neither related to the prevalence of MI nor to left ventricular function after MI.
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November 2004
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Research Article|
October 26 2004
Lack of association of a 9 bp insertion/deletion polymorphism within the bradykinin 2 receptor gene with myocardial infarction
Marcus FISCHER;
Marcus FISCHER
*Clinic for Internal Medicine 2, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany
†Human and Molecular Genetics Center, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A.
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Wolfgang LIEB;
Wolfgang LIEB
‡Clinic for Internal Medicine 2, University of Schleswig-Holstein, Ratzeburger Allee 160, 23538 Luebeck, Germany
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Daniel MAROLD;
Daniel MAROLD
*Clinic for Internal Medicine 2, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany
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Matthias BERTHOLD;
Matthias BERTHOLD
*Clinic for Internal Medicine 2, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany
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Andrea BAESSLER;
Andrea BAESSLER
*Clinic for Internal Medicine 2, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany
†Human and Molecular Genetics Center, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, U.S.A.
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Hannelore LOWEL;
Hannelore LOWEL
§GSF – Institute for Epidemiology, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany
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Hans-Werner HENSE;
Hans-Werner HENSE
∥Institute for Epidemiology, University of Münster, Domagkstr. 3, 48149 Münster, Germany
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Christian HENGSTENBERG;
Christian HENGSTENBERG
*Clinic for Internal Medicine 2, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany
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Stephan HOLMER;
Stephan HOLMER
*Clinic for Internal Medicine 2, University of Regensburg, Franz-Josef-Strauss Allee 11, 93053 Regensburg, Germany
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Heribert SCHUNKERT;
Heribert SCHUNKERT
‡Clinic for Internal Medicine 2, University of Schleswig-Holstein, Ratzeburger Allee 160, 23538 Luebeck, Germany
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Jeanette ERDMANN
‡Clinic for Internal Medicine 2, University of Schleswig-Holstein, Ratzeburger Allee 160, 23538 Luebeck, Germany
Correspondence: Dr Jeanette Erdmann (email [email protected]).
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Publisher: Portland Press Ltd
Received:
April 29 2004
Revision Received:
June 21 2004
Accepted:
August 05 2004
Accepted Manuscript online:
August 05 2004
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2004
Clin Sci (Lond) (2004) 107 (5): 505–511.
Article history
Received:
April 29 2004
Revision Received:
June 21 2004
Accepted:
August 05 2004
Accepted Manuscript online:
August 05 2004
Citation
Marcus FISCHER, Wolfgang LIEB, Daniel MAROLD, Matthias BERTHOLD, Andrea BAESSLER, Hannelore LOWEL, Hans-Werner HENSE, Christian HENGSTENBERG, Stephan HOLMER, Heribert SCHUNKERT, Jeanette ERDMANN; Lack of association of a 9 bp insertion/deletion polymorphism within the bradykinin 2 receptor gene with myocardial infarction. Clin Sci (Lond) 1 November 2004; 107 (5): 505–511. doi: https://doi.org/10.1042/CS20040129
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