gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Angiotensin II potentiates endothelin-1-induced vasoconstriction in the skin microcirculation of young, healthy men via angiotensin II receptors

Angiotensin II potenziert die Endothelin-1-induzierte Vasokonstriktion in der Haut-Mikrozirkulation junger, gesunder Männer über Angiotensin II Rezeptoren

Meeting Abstract

  • U. Rushentsova - Universitätsklinikum Essen (Essen, D)
  • A. Mitchell - Universitätsklinikum Essen (Essen, D)
  • R. Wenzel - Allgemeines öfftenliches Krankenhaus Zell am See, (Zell am See, A)
  • T. Philipp - Universitätsklinikum Essen (Essen, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP137

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Veröffentlicht: 8. August 2006

© 2006 Rushentsova et al.
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Background: We investigated the influence of subthreshold doses of angiotensin II (ATII) and noradrenaline (NA) on endothelin- (ET-1)-induced vasoconstriction, as well as the additional effects of ATII receptor antagonism on the skin microcirculation, to further define interactions of the blood pressure regulating systems.

Study design and methods: 15 healthy men (30±4 years) were included in this double blind, placebo controlled, randomised study. We used a Laser Doppler imager (moor LDI V 3.0) and the double injection technique to measure skin blood flow. We injected ATII (10-20 mol) and NA (10-19 mol) alone and combined with ET-1 (10-12,10-14,10-16 mol), as well as ET-1 alone (10-12,10-14,10-16 mol), following oral intake of either placebo (PLAC) or the AT1 receptor antagonist valsartan (VALS). Vasodilation to double injections of saline was used as baseline. Data were analyzed with ANOVA and are expressed as arbitrary perfusion units (PU, mean± SEM).

Results: Neither ATII (10-20 mol) nor NA (10-19 mol) alone altered baseline skin perfusion (ATII -7±11 PU, NA -3±14 PU). However, when injected in combination with ET-1, ATII significantly potentiated mean vasoconstriction to ET-1 (ET-1/PLAC: -59±19 PU vs. ATII+ET-1/PLAC: -107±22 PU, P= 0.029). In contrast, NA did not influence vasoconstriction to ET-1. Following valsartan, ET-1 induced vasodilation instead of vasoconstriction (ET-1/VALS: +77±36 PU, P< 0.001 vs. ET-1/PLAC). This valsartan effect was enhanced in a supra-additive fashion where ET-1 and ATII were combined (ATII+ET-1/VALS: +151±68 PU, P< 0.001 vs. ET-1/PLAC and vs. ATII+ET-1/PLAC).

Conclusion: AT II but not NA potentiates ET-1-mediated vasoconstriction in the skin microcirculation of young, healthy men in vivo. AT1 receptors are at least partly responsible for this effect. The vasodilation induced by ET-1 and to an even greater degree by ATII+ET-1 when AT1 receptors were blocked, suggests that other pathways, possibly via AT2 receptors, must be involved.