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The Glu27 allele of the beta2 adrenergic receptor increases the risk of cardiac hypertrophy in hypertension

Authors :
Guido Iaccarino
Ersilia Cipolletta
Raffaele Izzo
Valentina Trimarco
Nicola De Luca
Gianni Luigi Iovino
Francesca Lanni
Bruno Trimarco
Iaccarino, Guido
Francesca, Lanni
Ersilia, Cipolletta
Trimarco, Valentina
Izzo, Raffaele
Gianni Luigi, Iovino
DE LUCA, Nicola
Trimarco, Bruno
Source :
Journal of hypertension. 22(11)
Publication Year :
2004

Abstract

OBJECTIVE: Cardiac and vascular remodeling occur in response to hypertension. Genetic background appears to modify the development of target organ damage (TOD). We evaluated the impact on hypertension-associated TOD of a highly polymorphic gene with elevated significance for the regulation of the cardiovascular system, the beta2AR gene. METHODS: We recruited 775 hypertensives (mean +/- SE: age 53.5 +/- 0.5, from 20 to 84 years; female 32.7\%; systolic (SBP)/diastolic (DBP) blood pressure: 159 +/- 1.2/101 +/- 0.6 mmHg) referred to the departmental outpatient clinic and screened them for the Arg16Gly, Gln27Glu, and Ile164Thr variants of beta2AR gene. We performed association analyses on clinical, anamnesis, anthropometrical and biochemical parameters as well as cardiac and vascular ultrasound. RESULTS: We found that the three polymorphisms did not affect blood pressure levels. Cardiac TOD appeared to be related to the Glu27 variant. In fact, the Glu27 allele associates with a 1.4-fold higher risk of developing cardiac hypertrophy, and directly correlated with larger systolic and diastolic left ventricle internal diameters. Vascular TOD was not affected by the three polymorphisms. Ancillary to our finding we observed that the Glu27 variant is associated with a higher incidence of dyslipidemia. CONCLUSIONS: Our data indicate that beta2AR gene polymorphisms participate in the determination of cardiac TOD associated with hypertension.

Details

ISSN :
02636352
Volume :
22
Issue :
11
Database :
OpenAIRE
Journal :
Journal of hypertension
Accession number :
edsair.doi.dedup.....e1ff8c456a85aba9a362102d8836f69c