© 2003 European Society of Cardiology
Endothelial dysfunction in congestive heart failure: ACE inhibition vs. angiotensin II antagonism
a Medizinische Klinik der Julius-Maximilians-Universität Würzburg Josef Schneider Str. 2, D-97080 Würzburg, Germany
b Klinik für Anaesthesiologie der Julius-Maximilians-Universität Würzburg D-97080 Würzburg, Germany
* Corresponding author. Tel.: +49-931-201-1; fax: +49-931-201-36302. E-mail address: bauersachs_j{at}medizin.uni-wuerzburg.de
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Abstract |
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Background: Endothelial dysfunction of the vasculature contributes to the elevated peripheral resistance and reduced myocardial perfusion in congestive heart failure (CHF). The present study systematically investigated the effect of angiotensin II (AT1)- receptor blockade on vascular superoxide (O2–) production and endothelial dysfunction.
Methods and results: Vasodilator responses and O2– production were determined in aortic rings from Wistar rats with experimental CHF 10 weeks after extensive myocardial infarction and compared with sham-operated animals (Sham). Rats were either treated with placebo (P), with the AT1-receptor antagonist Irbesartan (50 mg kg–1 day–1) or with the ACE inhibitor Trandolapril (0.3 mg kg–1 day–1). In CHF-P, endothelium-dependent, acetylcholine-induced relaxation was significantly attenuated compared with Sham-P. Chronic treatment with Trandolapril or Irbesartan significantly improved endothelium-dependent relaxation. Aortic O2– formation was markedly increased in CHF, and was not significantly affected by Trandolapril treatment, while it was reduced by Irbesartan. eNOS expression was reduced in CHF and normalised by both treatments.
Conclusion: Endothelial vasomotor function in CHF rats was normalised by long-term treatment with an ACE inhibitor or an AT1-antagonist. Reduced aortic eNOS expression was normalised by both treatments, whereas aortic superoxide formation was only reduced by the AT1-antagonist Irbesartan.
Key Words: Endothelium • Angiotensin • Myocardial infarction • Free radicals
Received June 13, 2003; Revised August 17, 2003; Accepted October 23, 2003
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