gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

Angiotensin II modulates renal sympathetic neurotransmission through nitric oxide in AT2 receptor knockout mice

In AT2 Knockout Mäusen moduliert Angiotensin II durch NO die renale sympathische Neurotransmission

Meeting Abstract (Hypertonie 2004)

  • J. Stegbauer - Marienhospital Herne (Herne, D)
  • O. Vonend - Marienhospital Herne (Herne, D)
  • S. Habbel - Marienhospital Herne (Herne, D)
  • I. Quack - Marienhospital Herne (Herne, D)
  • L.C. Rump - Marienhospital Herne (Herne, D)

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP62

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2004/04hoch062.shtml

Veröffentlicht: 10. August 2005

© 2005 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

Angiotensin (Ang) II enhances renal sympathetic neurotransmission and stimulates NO release. The present study investigates whether Ang II mediated modulation of sympathetic neurotransmission is dependent on NO production in the kidney. AT2 -/y receptor deficient mice are used to identify the Ang II receptor subtype involved. Mice kidneys were isolated and perfused with Krebs-Henseleit solution. Drugs were added to the perfusion solution in a cumulative manner. Release of endogenous norepinephrine (NE) was measured by HPLC. AT1-receptor expression was analysed by real time PCR. Ang II (0.01 nM - 30 nM) dose dependently increased pressor responses in kidneys of AT2 -/y mice and wild type (AT2 +/y) mice. Maximal pressor responses and EC50 values for Ang II and NE were greater in AT2 -/y than in AT2 +/y mice. L-NAME (0.3 mM) enhanced Ang II induced pressor responses in both strains. In AT2 -/y mice Ang II induced facilitation of NE release was more pronounced than in AT2 +/y mice. L-NAME reduced Ang II mediated facilitation of NE release in both strains. This reduction was more potent in AT2 -/y mice. In kidneys of AT2 -/y mice the AT1 receptor expression was upregulated. These results suggest that activation of AT1 receptors by Ang II releases NO in mouse kidney to modulate sympathetic neurotransmission. Since AT1 receptors are upregulated in AT2 -/y mice kidneys, NO dependent effects were greater in these mice. Thus, NO seems to play an important modulatory role for renal sympathetic neurotransmission.