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

Effect of angiotensin II on mediators of inflammation in healthy volunteers

Wirkung von Angiotensin II auf Entzündungsmediatoren bei gesunden Probanden

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker K. Lottermoser - Medizinische Universitäts-Poliklinik (Bonn, D)
  • G. Ulrich-Merzenich - Medizinische Universitäts-Poliklinik (Bonn, D)
  • H. Vetter - Medizinische Universitäts-Poliklinik (Bonn, D)
  • R. Düsing - Medizinische Universitäts-Poliklinik (Bonn, D)

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP94

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

Published: November 11, 2004

© 2004 Lottermoser 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.




Inflammatory reactions, mediated by cytokines, are of major importance in the development of atherosclerotic lesions. Several experimental studies suggest a relationship between the renin-angiotensin-aldosterone system and the release of cytokines from the endothelium. The present study was designed to further evaluate this hypothesis in healthy volunteers.


Angiotensin II was infused intravenously in nine healthy volunteers in graded doses of 1, 3 and 10 ng/kg/min, each for 45`, without and with AT1-receptor blockade (Valsartan, 160mg). Blood for the determination of angiotensin II and the proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and the vascular cell adhesion molecule (VCAM)-1 was taken before the start of the infusion, at the end of each infusion period and 1h after the infusion was stopped.


During the infusion periods, angiotensin II plasma concentrations increased from 14.7 ± 5.5 pg/ml to a maximum of 200.1 ± 42.4 pg/ml (p<0.001). One hour after the infusion, plasma angiotensin II concentrations had returned into the control range (16.3 ± 7.6 pg/ml). Systolic and diastolic blood pressure were increased by angiotensin II from 121 ± 3/70 ± 2 mmHg to a maximum of 146 ± 2/97 ± 1 mmHg (p<0.001). AT1-receptor blockade prevented that increase in blood pressure. Neither during the infusion of angiotensin II alone nor with additional AT1-receptor blockade, any change in circulating plasma levels of TNF-alpha, IL-6 or VCAM-1 could be seen.


Though increased circulating levels of angiotensin II induce a significant increase in arterial blood pressure, they are not followed by short-term changes in plasma levels of the cytokines that were determined in the actual study. Our results in healthy volunteers question the concept that angiotensin II mediates short-term blood-pressure-independent effects by influencing TNF-alpha, IL-6 or VCAM-1.