gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Effects of the Gln27Glu- and the Arg16Gly-beta2-adrenoceptor polymorphisms on agonist-induced desensitization of beta2-adrenoceptor-mediated venodilation in vivo

Einfluß der Gln27Glu- und Arg16Gly-Beta2-Adrenozeptor Polymorphismen auf die Agonist-induzierte Desensibilisierung der beta2-Adrenozeptor vermittelten Venendilatation in vivo

Meeting Abstract (Hypertonie 2004)

  • H. Bruck - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • J. Park - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • K. Leineweber - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • O.-E. Brodde - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • T. Philipp - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP69

The electronic version of this article is the complete one and can be found online at:

Published: August 10, 2005

© 2005 Bruck et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Background: Beta2-adrenoceptors (AR) are polymorphic. In vitro agonist-induced desensitization is blunted with the Gln27Glu and enhanced with Arg16Gly polymorphism compared to wild-type (WT) beta2AR. We have found that, in vivo in healthy volunteers, these polymorphisms do not influence agonist-induced desensitization of cardiac ß2-AR responses, but the Glu27 variant slows the onset of desensitization.

Methods: We studied terbutaline (TER 50, 100, 200, 400, 1000 ng/min) induced venodilation of a phenylephrine-induced 60%-preconstricted dorsal hand vein in 10 volunteers homozygous for the WT beta2AR (i.e. homozygous Arg16 and Gln27, group A) and 9 volunteers homozygous Glu27 (and homozygous Gly16, group B) and 8 subjects homozygous Gly16 (and homozygous Gln27, group C) at baseline and after 2 weeks treatment with 3x5mg terbutaline/ day- a treatment which has been shown to desensitize beta2AR responses.

Results: At baseline, TER induced a dose-dependent, significant venodilation in all three groups. Maximum venodilation was 74±3% (A), 72±4% (B) and 75±4% (C) and not significantly different between the 3 groups. After 15 days of TER-treatment, TER-induced venodilation was significantly blunted in WT-volunteers (group A: 58±4%, p<0.0001 vs. baseline) and volunteers with the Gly16 polymorphism (with Gln27, group C: 66±8%, p=0.01 vs. baseline). In contrast, in volunteers with the Glu27 (with Gly16) polymorphism 2 weeks TER-treatment had no significant effect on dose-response curve of TER-induced venodilation (group B: 69±6%, n.s. vs. baseline).

Conclusion: These data indicate that the ß2-AR mediated dorsal hand vein dilation undergoes agonist-promoted desensitization only in WT- and Gly16-ß2-AR but not in Glu27-ß2-AR volunteers. Thus, in heart and dorsal hand vein agonist-induced desensitization pattern of the Glu27-ß2-AR polymorphism is altered: in heart the desensitization process is slowed, in the dorsal hand vein it is (during 2 wks agonist-treatment) absent.