SUPEROXIDE ANIONS AND HYPEROXIA INACTIVATE ENDOTHELIUM-DERIVED RELAXING FACTOR
SUPEROXIDE ANIONS AND HYPEROXIA INACTIVATE ENDOTHELIUM-DERIVED RELAXING FACTOR
复制标题
DOI:
10.1152/ajpheart.1986.250.5.h822
复制
发表时间:
1986-05-01
影响因子:
--
通讯作者:
VANHOUTTE, PM
中科院分区:
文献类型:
--
作者:
RUBANYI, GM;VANHOUTTE, PM
Experiments were designed to determine the effects of oxygen-derived free radicals on the production and biological activity of endothelium-derived relaxing factor or factors released by acetylcholine. Rings of canine coronary arteries without endothelium (bioassay rings) were superfused with solution passing through a canine femoral artery with endothelium. Superoxide dismutase caused maximal relaxation of the bioassay ring when infused upstream, but not downstream, of the femoral artery; this effect of superoxide dismutase was inhibited by catalase. Infusion of acetylcholine relaxed the bioassay rings because it released a labile relaxing factor (or factors) from the endothelium. When infused below the femoral artery, superoxide dismutase and, to a lesser extent, catalase augmented the relaxations to acetylcholine. Superoxide dismutase, but not catalase, doubled the half-life of the endothelium-derived relaxing factor(s). This protective effect of the enzyme was augmented fivefold by lowering the oxygen content of the perfusate from 95 to 10%. These data demonstrate that: (1) superoxide anions inactivate the relaxing factor(s) released by acetylcholine from endothelial cells and (2) hyperoxia favors the inactivation of endothelium-derived relaxing factor(s).