Isoform-specific differences in the nitrite reductase activity of nitric oxide synthases under hypoxia.

摘要: Nitrite (NO(2)(-)) recycling to nitric oxide (NO) is catalysed by a number of enzymes and induces protective vasodilation effect under hypoxia/ischaemia. In the present work, we tested in vitro ability three NOS (nitric synthase) isoforms release NO from nitrite anoxia using electrochemical detection, chemiluminescence absorption spectroscopy. The free anoxic solutions at 15 muM was specific endothelial isoform (eNOS) did not occur with neuronal (nNOS) or inducible (iNOS) isoforms. Unlike xanthine oxidase, eNOS reductase domain recycle NO, wild-type reduce nitrate. Our data suggest that structural and, inference, dynamic differences between nNOS distal haem side account for being only capable converting into pH 7.6. human dermal microvascular cells careful control oxygen tension, rates formation determined were enhanced approximately 3.6- 8.3-fold hypoxia (2 p.p.m. O(2)) (argon) respectively compared normoxia ( 22 10 extracellular nitrite. inhibitors inhibited this hypoxic release. show unique it releases all levels complete physiological micromolar concentrations. magnitude endothelium could provide an appropriate response acute episodic ischaemia may explain observed eNOS-expression-specific as short-term animal models hypoxia.