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 |
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Sprache: | eng |
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