Endothelial dysfunction in congestive heart failure: ACE inhibition vs. angiotensin II antagonism

摘要: Background: Endothelial dysfunction of the vasculature contributes to elevated peripheral resistance and reduced myocardial perfusion in congestive heart failure (CHF). The present study systematically investigated effect angiotensin II (AT1)- receptor blockade on vascular superoxide (O2−) production endothelial dysfunction. Methods results: Vasodilator responses O2− were determined aortic rings from Wistar rats with experimental CHF 10 weeks after extensive infarction compared sham-operated animals (Sham). Rats either treated placebo (P), AT1-receptor antagonist Irbesartan (50 mg kg−1 day−1) or ACE inhibitor Trandolapril (0.3 day−1). In CHF-P, endothelium-dependent, acetylcholine-induced relaxation was significantly attenuated Sham-P. Chronic treatment improved endothelium-dependent relaxation. Aortic formation markedly increased CHF, not affected by treatment, while it Irbesartan. eNOS expression normalised both treatments. Conclusion: Endothelial vasomotor function long-term an AT1-antagonist. Reduced treatments, whereas only AT1-antagonist