gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Angiotensin II-induced vasoconstriction can be affected by coactivation of P2Y-Receptors

Die Angiotensin II induzierte Vasokonstriktion egulation und Steuerung der Endothelfunktion eine Rolle

Meeting Abstract (Hypertonie 2004)

Suche in Medline nach

  • M. Tölle - Med. Klinik IV - Charité, Campus Benjamin Franklin (Berlin, D)
  • W. Zidek - Med. Klinik IV - Charité, Campus Benjamin Franklin (Berlin, D)
  • M. van der Giet - Med. Klinik IV - Charité, Campus Benjamin Franklin (Berlin, D)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP116

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2004/04hoch116.shtml

Veröffentlicht: 10. August 2005

© 2005 Tölle 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

Text

In the last years there is increasing evidence that purinergic signalling is involved in blood pressure control. Activation of P2Y-receptors is coupled to activation of Rho-kinase and consecutively to increase of the phosphorylated form of myosin-light chain (MLC). This effect is called "calciumsensitization". In the present study we investigated known purinergic agonists, i.e. UTP and UDP, to study their effects on calciumsensitization. We wanted to show whether the presence of nucleotides leads to an increase in vasoactive properties of the known vasoactive peptide Angiotensin II.

We used the isolated perfused rat kidney to study the influence of the presence of UTP or UDP on AngII-induced vasoconstriction.

Results: Single doses of Ang II, UDP and UTP induced a dose-dependent vasoconstriction in the isolated perfused rat kidney (ED50 [-log mol]: AngII 10.9±0.1; UTP 5.0±0.2 and UDP 5.0±0.1). Permanent perfusion with UTP or UDP did not show any vasoconstriction with concentrations below 1 µM. In the presence of UTP or UDP, dose-response curves of Ang II were significantly shifted to the left at concentrations higher than 100 pM for UTP and UDP. The dose-response shift for Ang II was maximum for concentrations of 10 nM for UDP (ÉD50: Ang II+UDP (10 nM): 11.5±0.1) and 10 nM UTP (EC50: Ang II+UTP (10 nM): 11.7±0.2). In the presence of reactive blue (10 µM), a P2Y-receptor antagonist, or pyridoxalphosphate-azophenol-disulfonic acid (PPADS, 10 µM), neither UTP nor UDP shiftet the Ang II dose-response curve to the left. The Rho-kinase inhibitor Y-27632 (10 µm) reveresed the UTP and UDP induced shift of AngII-induced dose reponse curve.

UTP and UDP can augment AngII-induced vasoconstriction in nmolar concentrations. It could be demonstrated that the UTP and UDP-induced change in vasoacitivity of Ang II is induced by P2Y-receptoractivation and Rho-kinase activation. Purinergic agonists activating P2Y-receptors might play an important in indirect blood pressure regulation.