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Valsartan and candesartan can inhibit deteriorating effects of angiotensin II on coronary endothelial function
Author(s) -
Harald Seeger,
C Lippert,
D. Wallwiener,
Alfred O. Mueck
Publication year - 2001
Publication title -
journal of the renin-angiotensin-aldosterone system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 46
eISSN - 1752-8976
pISSN - 1470-3203
DOI - 10.3317/jraas.2001.016
Subject(s) - candesartan , valsartan , angiotensin ii , medicine , endocrinology , endothelin receptor , bradykinin , receptor , angiotensin receptor , angiotensin ii receptor type 1 , quinapril , plasminogen activator , chemistry , renin–angiotensin system , pharmacology , blood pressure , angiotensin converting enzyme , ace inhibitor
The angiotensin II (Ang II) AT 1 -receptor antagonists, valsartan and candesartan, were compared with regard to their effect on Ang II-mediated changes in parameters of coronary endothelial function. Ang II (10 µM) induced increased concentrations of the vasoconstrictor endothelin, the procoagulatory substance plasminogen-activator-inhibitor-1 (PAI-1) and the precursor of the matrix-metalloproteinase 1 (MMP-1) in endothelial cell cultures from human coronary arteries. These increases were completely prevented by the addition of 10 µM valsartan or candesartan and partially by the addition of lower concentrations of these drugs, i.e. 1 µM and 0.1 µM. No significant difference between the effect of the two AT 1 -receptor antagonists was observed. These results suggest that AT 1 -receptor antagonists not only can reduce blood pressure by blocking the action of Ang II, but might also contribute to the prevention of atherogenesis and plaque instability.

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