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

Improvement of endothelial function in diabetes mellitus: AT1 receptor antagonism vs. beta receptor blockade

Verbesserung der endothelialen Funktion bei Diabetes mellitus: AT1-Rezeptorantagonismus versus Betarezeptor-Blockade

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker M. Dorenkamp - Charité - Campus Benjamin Franklin, Cardiology (Berlin, D)
  • A. Riad - Charité - Campus Benjamin Franklin, Cardiology (Berlin, D)
  • D. Westermann - Charité - Campus Benjamin Franklin, Cardiology (Berlin, D)
  • H.P. Schultheiss - Charité - Campus Benjamin Franklin, Cardiology (Berlin, D)
  • C. Tschöpe - Charité - Campus Benjamin Franklin, Cardiology (Berlin, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP60

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

Published: November 11, 2004

© 2004 Dorenkamp 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.



Endothelial dysfunction (ED) is an initial step in vascular disease and often present in diabetes mellitus. We wanted to determine the effects of angiotensin type-1 receptor antagonists (AT1A) and beta blockers (BB) on ED in diabetic rats.

Experiments were performed in streptozotocin (STZ)-induced diabetic Sprague Dawley (SD) rats treated with the AT1A candesartan (Can) (1mg/kg/d), or the BB metoprolol (Met) (30mg/kg/d) or vehicle and in age matched controls (n=9/group). Vasoactive responses were studied in in situ autoperfused hindquarters. The endothelial-dependent vasodilation was analyzed by induction of shear stress (S) by injection of Krebs-Henseleit solution (200µl/kg) and the non-endothelial-dependent dilation by application of sodium nitroprusside (SNP, 40µg/kg). Immunohistochemically intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 were quantified in relation to net quadriceps muscle area.

The vasodilatory endothelial-dependent and non-endothelial-dependent responses of SD-STZ were impaired compared to controls (S: amplitude (mmHg): 22.9±1.9 vs. 51.2±3; Integral (mmHg*s): 1093±83 vs. 2450±312; SNP: Integral (mmHg*s): 3638±671 vs. 6602±953; p<0.05). This was accompanied with an increased expression of ICAM-1 and VCAM-1 (Area fraction: 0.61±0.14 vs. 0.09±0.01 and 0.52±0.1 vs. 0.06±0.01; p<0.05). The endothelial-dependent response of SD-STZ-Can but not of SD-STZ-Met was improved compared to SD-STZ (Can: S: Amplitude: 38.9±3.1 vs. 22.9±1.9; Integral: 1844±160 vs. 1093±83; p<0.05; Met: S: Amplitude: 23.7±2.2 vs. 22.9±1.9; Integral: 1430±157 vs. 1093±83; n.s.). Neither Can nor Met improved the non-endothelial-dependent response. Can suppressed the expression of VCAM-1 (0.07±0.01 vs. 0.52±0.1; p<0.05) but not of ICAM-1. Met had no effect on immunoreactivity.

Treatment with Can but not with Met shows vascular-protective effects in diabetic ED. As VCAM-1 expression is decreased, Can may elicit anti-inflammatory mechanisms.