gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Endothelin- and angiotensin II- antagonism inhibit the systemic hemodynamic response to exogenous noradrenaline

Meeting Abstract (Hypertonie 2004)

  • A. Mitchell - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • A. Ferraioli - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • U. Rushentsova - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • J. Nürnberger - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • R. Schäfers - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • T. Philipp - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • R. Wenzel - Krankenhaus Zell am See A

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP70

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2004/04hoch070.shtml

Veröffentlicht: 10. August 2005

© 2005 Mitchell et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

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Background: Both stimulation and inhibition of the various components of blood pressure (BP) control may be the result of interactions of the BP-regulating systems. We performed this study to characterize the influence of the Endothelin (ET)-system and the renin-angiotensin- system on sympathetically mediated vasoconstriction.

Methods: 7 young, healthy men were investigated in a randomised, placebo-controlled, double-blind, cross-over study. They received either placebo, the angiotensin II (ATII)- receptor antagonist candesartan (8 mg orally) or the ET-A-selective antagonist BQ123 (60 ug/min iv.) with subsequent infusion of noradrenaline (NA 20-160 ng/kg/min). Hemodynamic measurements were performed at baseline, after 3.5 h and after each NA dose. Statistical significance was assessed by t-test or two-way ANOVA.

Results: Following application of placebo BP rose dose dependently in response to NA-infusion (max. rise in systolic BP 46±5 mmHg, max. rise in diastolic BP: 16±4 mmHg (mean ± SEM, P= 0.0001 and P= 0.011 vs. baseline). The NA-induced effect on systolic BP was inhibited by BQ123 (P= 0.002 vs. placebo) as well as by candesartan (P= 0.004 vs. placebo) with no difference between the responses to these drugs (P= 0.67 for candesartan vs. BQ123). The NA-induced change in diastolic BP was also reduced by ET-A- and AT II-receptor blockade, but this was not statistically significant. The rise in BP was accompanied by a fall in heart rate that was similar for placebo and candesartan but was significantly less for BQ123 (P= 0.013 and P= 0.004 for BQ123 vs. candesartan and BQ123 vs. placebo).

Conclusion: AT1- antagonism and ET-A-antagonism reduce the hemodynamic response to exogenous alpha-adrenergic stimulation. The difference between candesartan and BQ123 in heart rate response may reflect a differential influence of the drugs on central sympathetic tone.