Reduced agonist-induced endothelium-dependent vasodilation in uremia is attributable to an impairment of vascular nitric oxide

Current concepts for the explanation of endothelial dysfunction and accelerated atherosclerosis in uremia propose a reduced vascular bioavailability of nitric oxide (NO). The aim of the present study was to test the contributions of NO and NO/prostacyclin (PGI(2))-independent mechanisms to both base...

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Veröffentlicht in:Journal of the American Society of Nephrology 2005-04, Vol.16 (4), p.959-965
Hauptverfasser: Passauer, Jens, Pistrosch, Frank, Büssemaker, Eckhart, Lässig, Grit, Herbrig, Kay, Gross, Peter
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Sprache:eng
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