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 induced renal vasoconstriction is modulated by endothelial derived nitric oxide in mice

Endothelial derived Nitric Oxide moduliert in Mäusen die Angiotensin II induzierte renale Vasokonstriktion

Meeting Abstract

  • J. Stegbauer - Klinikum der Ruhr-Universität Bochum, Marienhospital Herne (Herne, D)
  • O. Vonend - Klinikum der Ruhr-Universität Bochum, Marienhospital Herne (Herne, D)
  • L.C. Rump - Klinikum der Ruhr-Universität Bochum, Marienhospital Herne (Herne, D)
  • Y. Kuczak - Joahnnes-Müller-Institut für Physiologie, Humboldt-Universität Berlin (Berlin, D)
  • A. Patzak - Joahnnes-Müller-Institut für Physiologie, Humboldt-Universität Berlin (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP180

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2005/05hoch180.shtml

Veröffentlicht: 8. August 2006

© 2006 Stegbauer 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

Objective: Nitric oxide (NO) modulates Angiotensin (Ang) II induced renal vasoconstriction in mice. NO is generated by endothelial nitric oxide synthase (eNOS) or neuronal nitric oxide synthase (nNOS). Therefore, the present study investigated whether this effect is due to endothelial-derived NO or whether the neuronal NOS isoform located in the macula densa cells is responsible for counteracting Ang II induced vasoconstriction. Mice that are homozygous (-/-) for disruption of the eNOS or the nNOS gene were used to examine effects of selectively inhibited NO production by either eNOS or nNOS.

Design and Methods: Mice were anaesthesized and renal arteries were cannulated through the abdominal aorta. The kidneys were then perfused with Krebs-Henseleit solution (7.25 ml/min/g kidney wet weight). Drugs were added to the perfusion solution in a cumulative manner or throughout. Perfusion pressure was monitored continuously.

Results: Ang II increased renal vascular tone in kidneys of eNOS (-/-), nNOS (-/-) and wild type (WT) mice. Maximal pressor responses and EC50 to Ang II were significant greater in eNOS (-/-) than in WT mice. The nonselective NO synthase inhibitor L-NAME (0.3 mM) enhanced the Ang II induced pressor response in nNOS (-/-) and WT mice significantly, whereas no significant change in pressor response were seen in kidneys of eNOS (-/-) mice. 7-nitroindazole monosodium salt, the selective nNOS inhibitor 7-NINA has no significant effect on Ang II induced pressor response in kidneys of eNOS (-/-), nNOS (-/-) and wild type mice.

Conclusion: The present study could demonstrate that NO is important for modulating Ang II induced pressor response in mice kidneys. Moreover, this effect seems to be regulated exclusively by the endothelial NOS, whereas the neuronal NOS has shown no effect on Ang II induced renal vasoconstriction in mice