gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Beta2-adrenoceptor mediated intrinsic sympathomimetic activity of carteolol: an in vivo study

Beta2-Adrenozeptor vermittelte intrinsische sympathomimetische Aktivität von Carteolol: eine in vivo Studie

Meeting Abstract (Hypertonie 2004)

  • H. Bruck - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • U. Poller - Universitätsklinikum Halle
  • H. Lüssenhop - Universitätsklinikum Halle
  • K. Pönicke - Universitätsklinikum Halle
  • T. Temme - 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. Doc04hochP68

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: The intrinsic sympathomimetic activity (ISA) of a beta-adrenoceptor blocker can be mediated by beta1- or beta2-adrenoceptors. The aim of this study was to characterize, in healthy volunteers, the ISA of the beta-adrenoceptor blocker carteolol.

Methods: Two approaches were employed: 1) we assessed in the volunteers the effects of carteolol (20, 40 or 80 mg p.o.) on blood pressure, heart rate and heart-rate corrected duration of electromechanical systole (QS2c - as a measure of cardiac contractility).

Results: Carteolol dose-dependently increased systolic blood pressure, heart rate and contractility and decreased diastolic blood pressure. The beta1-adrenoceptor blocker bisoprolol did not attenuate these carteolol effects, but rather enhanced the effects on heart rate and systolic blood pressure. 2) We treated volunteers for seven days with 1x20 mg/day carteolol and assessed lymphocyte beta2-adrenoceptor density (by ICYP binding) and functional responsiveness (by 10 mM isoprenaline-induced increase in lymphocyte cyclic AMP content). Carteolol significantly reduced lymphocyte beta2-adrenoceptor density and function; however, after withdrawal of carteolol lymphocyte beta2-adrenoceptor density and function did only very slowly recover and even 11 days after carteolol withdrawal had not returned to control levels.

Conclusion: On the one side, the cardiovascular effects of carteolol were resistant against the beta1-adrenoceptor blocker bisoprolol and, on the other hand, carteolol significantly decreased lymphocyte beta2-adrenoceptor density and function. These results are in favour of the idea that the ISA of carteolol is mediated by beta2-adrenoceptors. Involvement of an additional receptor site (e.g. the propranolol-resistant state of the beta1-adrenoceptor), however, cannot be excluded.