gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Deficiency for the G protein-coupled receptor Mas prevents inversion of circadian rhythmus by Angiotensin II

Defizienz für den G-Protein gekoppelten Rezeptor Mas verhindert die Inversion des zirkadianen Rhythmus nach Angiotensin II-Gabe

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker S. Heringer-Walther - UKBF (Berlin, D)
  • H.P. Schultheiss - UKBF (Berlin, D)
  • T. Walther - UKBF (Berlin, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP41

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2003/03hoch141.shtml

Veröffentlicht: 11. November 2004

© 2004 Heringer-Walther 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

The Mas protooncogene encodes a G protein-coupled receptor with seven transmembrane domains and has been discussed as an angiotensin (Ang) II receptor. Recently, we demonstrated that Ang-(1-7) is a functional ligand for this receptor (Santos et al., PNAS 2003).

To investigate the role of Ang II and Mas in blood pressure control under physiological conditions, Mas-deficient mice were analysed using radiotelemetry. Six female Mas-knockout (KO) mice and 8 controls (C) (10 months) received a telemetry implant (DSI, USA) in the carotid artery. All mice were housed in individual cages in light cycles (6am-6pm). After 1 week recovery, basal cardiovascular parameters were recorded for 3 days and subsequently Ang II (540ng/h) was continuously administered by osmotic minipumps for 5 days.

The 24h-basal mean arterial pressure (MAP) and heart rate (HR) were not different between KO and C (KO: 104.8+/-1.5 mmHg, 555+/-38 bpm; C: 105+/-1.4 mmHg, 572+/-48 bpm). The delta [night minus day (n-d)] of basal MAP and HR were also not different between KO and C (KO +7.9+/-0.6 mmHg, +37.2+/-13.6 bpm; C: +8.4+/-0.8 mmHg, +24+/-6.2 bpm). During the first 2 days of Ang II infusion, the 24-hour rhythm of MAP was inverted/blunted in C but not in KO (n-d1: KO +4.1+/-1.6 vs. C -2.3+/-1.4mmHg; n-d2: KO +7.7 +/-1.0 vs. C +2.3+/-1.7mmHg, P<0.05). There was no difference between the groups in the following days of infusion (n-d3: KO +5.9+/-2.8 vs. C +5.8+/-1.8mmHg; n-d4: KO +7.3+/-0.7 vs.C +9.7+/-2.2mmHg). In both, KO and C, the 24-hour HR rhythms remained unaltered.

These results demonstrate that Mas also plays a role in mediating the effects of Ang II on the circadian variation of blood pressure. Research into the mechanisms of Mas in the diurnal variations of cardiovascular regulation may lead to a better understanding of the pathogenesis of cardiovascular disorders and, hence, the emergence of novel therapeutic strategies for these diseases.