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

ACE inhibition normalizes altered expression patterns of ROS generating genes in glomerular proteinuria

ACE-Inhibition normalisiert veränderte Expressionsmuster ROS-bildender Gene in der glomerulären Proteinurie

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker M. Wehland-von Trebra - Charité-Universitätsmedizin Berlin (Berlin, D)
  • I. Oppong - Charité-Universitätsmedizin Berlin (Berlin, D)
  • M. Dierschke - Charité-Universitätsmedizin Berlin (Berlin, D)
  • R. Kreutz - Charité-Universitätsmedizin Berlin (Berlin, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP87

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Wehland-von Trebra et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Proteinuria and hypertension are the most important factors for the progression of renal disease and the development of terminal renal failure. To study the role of oxidative stress and reactive oxygen species (ROS) in the glomerulus we performed systematic expression analysis in the Munich Wistar Frömter rat (MWF). The MWF strain represents a suitable genetic model for increased albuminuria (proteinuria) and spontaneous arterial hypertension. We determined the expression of the NADPH subunits NOX1, NOX4, p22-phox, p47-phox, and rac1 as well as eNOS and iNOS in glomerular RNA with the TaqMan technique. All measurements were carried out in three groups consisting of untreated MWF, untreated Wistar control rats, and ACE-inhibitor (ACE-I) treated (between week 16 and 24 of age) MWF rats (n=8-12, respectively). Systolic blood pressure of unreated MWF (168 +- 3 mm Hg p<0.005 vs. Wis ) was normalized by ACE-I (129 +- 2 mm Hg) to normotensive Wis control levels (127 +- 2 mm Hg). ACE-I treatment was able to stop the progression of albuminuria in MWF, while no reversion to normal levels was observed. No change in expression between the three groups could be observed for the NOX1, NOX4, p22-phox, and rac1 genes, respectively. The cytosolic subunit p47-phox, however, was clearly elevated (2.3 fold, p<0.05 vs. Wis) in untreated MWF rats and its expression could be normalized by ACE-I treatment. NO synthase isoforms eNOS and iNOS showed a significant upregulation of in untreated MWF rats (199.4 +- 52.1 % and 243.5 +- 99.5 %, respectively; p<0.05 vs. Wis), whereas the ACE-I-treated group exhibited no difference in eNOS and iNOS levels compared to the healthy Wistar control rats. Our data hint towards an imbalanced expression of ROS-generating genes as well as eNOS and iNOS in the glomerulus of MWF, which is normalized by ACE-I treatment.