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Cardiovascular Research 2000 47(1):142-149; doi:10.1016/S0008-6363(00)00083-3
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Endothelin-receptor blockade improves endothelial vasomotor dysfunction in heart failure

Johann Bauersachs*, Daniela Fraccarollo, Paolo Galuppo, Julian Widder and Georg Ertl

Medizinische Klinik der Julius-Maximilians-Universität Würzburg and II. Medizinische Klinik, Universitätsklinikum Mannheim, Mannheim, Fakultät für Klinische Medizin Mannheim der Universität Heidelberg, Heidelberg, Germany

* Corresponding author. Present address: Medizinische Universitätsklinik, Josef-Schneider-Str. 2, D-97080 Würzburg, Germany. Tel.: +49-931-201-5301; fax: +49-931-201-5302 j.bauersachs{at}medizin.uni-wuerzburg.de

Objectives: To elucidate the effect of selective endothelin ETA- and mixed ETA/B-receptor antagonists on endothelial vasomotor dysfunction in rats with heart failure after myocardial infarction (MI). Methods: Vasoreactivity and superoxide anion formation were determined in aortic rings from Wistar rats 12 weeks after extensive MI (>46% of left ventricle) compared to sham-operated animals. Rats were either treated with the selective ETA-receptor antagonist LU 135252 (30 mg/kg/day), the mixed ETA/B-receptor antagonist Bosentan (100 mg/kg/day) or placebo. Results: In MI rats, the concentration–response curve of the endothelium-dependent, nitric oxide-mediated relaxation induced by acetylcholine was significantly shifted to the right and the maximum relaxation was attenuated. Long-term treatment with both ET antagonists significantly improved acetylcholine-induced relaxation in MI rats. LU 135252 was more effective than Bosentan. Endothelium-independent relaxations induced by sodium nitroprusside as well as endothelin- and phenylephrine-induced contractions were similar in all groups of rats. Plasma renin activity and aortic superoxide formation, which were enhanced in rats with heart failure, were normalized by LU 135252, but not by Bosentan treatment. Conclusions: Long-term treatment with ET-receptor antagonists improves endothelial vasomotor dysfunction in rats with chronic MI. This mechanism may essentially contribute to the beneficial effects of ET receptor blockade in heart failure.

KEYWORDS Endothelial function; Endothelins; Free radicals; Heart failure; Nitric oxide; Vasoconstriction/dilation


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