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Mueck AO et al.  
Comparison of Valsartan With Candesartan on Their Possible Protection From Atherosclerosis

Journal of Clinical and Basic Cardiology 2001; 4 (4): 297-299

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Fig. 1: AII-Antagonisten - Atherosklerose Fig. 2: AII-Antagonisten - Atherosklerose Fig. 3: AII-Antagonisten - Atherosklerose Fig. 4: AII-Antagonisten - Atherosklerose Fig. 5: AII-Antagonisten - Atherosklerose

Keywords: Angiotensin IIAtherogeneseCandesartanValsartanAngiotensin IIatherogenesisCandesartanValsartan

It is well appreciated that AT1-antagonists do diminish long-term effects of angiotensin on the blood pressure which are regarded as detrimental. In the present in vitro experiments we compared the efficacies of valsartan and candesartan in preventing negative outcomes of angiotensin effect on markers of endothelial function and on proliferation of smooth muscle cells. Angiotensin II (10 然) induced a decrease in the concentration of endothelial-derived nitric oxide synthase and increases the concentration of the vasoconstrictor endothelin, the procoagulatory substance plasminogen-activator-inhibitor-1 (PAI-1) and of the precursor of the matrix-metalloproteinase 1 (MMP-1) in endothelial cell cultures from human coronary arteries. These changes were completely prevented by the addition of 10 然 of valsartan or candesartan and partially by the addition of lower concentrations of the sartans, ie 1 然 and 0.1 然. No significant difference was observed in the effect of the two sartans. The angiotensin II-induced increase of coronary artery smooth muscle cell proliferation was also completely prevented by the addition of 10 然 of the sartans. These results suggest that sartans may class-specifically inhibit negative actions of angiotensin II on endothelial function and smooth muscle cell proliferation. Thus sartans may be able to prevent the initiation and progression of atherosclerosis.
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