Potential role of a membrane-bound NADH oxidoreductase in nitric oxide release and arterial relaxation to nitroprusside.
Potential role of a membrane-bound NADH oxidoreductase in nitric oxide release and arterial relaxation to nitroprusside.
复制标题
膜结合 NADH 氧化还原酶在一氧化氮释放和硝普钠动脉松弛中的潜在作用。
DOI：
10.1161/01.res.84.2.220
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发表时间：
1999
影响因子：
20.1
通讯作者：
Wolin,MS
中科院分区：
文献类型：
--
作者：
Mohazzab-H,KM;Kaminski,PM;Agarwal,R;Wolin,MS
-负责硝普钠释放一氧化氮(NO)的血管平滑肌代谢部位尚未完全确定。在这项研究中，我们观察到肺动脉膜上的NADH氧化还原酶激活硝普钠释放NO，我们研究了这一过程是否可能参与硝普钠的松弛。NO清除剂和NO拮抗剂对鸟氨酸环化酶的刺激均可抑制牛肺动脉对硝普钠的松弛作用。抑制肺动脉NADH氧化还原酶的黄素蛋白探针(1μ/L二苯基碘)和NADH氧化还原酶的电子受体(0.3mmoL/L硝基蓝四氮唑和0.1mmoL/L铁氰化物)可抑制硝普钠对肺动脉的松弛，但对硝酸甘油的松弛作用不明显。体外观察到肺动脉对硝普钠释放NO有促进作用，而硝基蓝四氮唑、铁氰化物和二苯基碘对NO的释放有抑制作用。在肺动脉匀浆中，NADH(0.1mmoL/L)使≈释放的NO增加6倍，而NADPH、线粒体底物和其他氧化还原辅因子对NO释放的影响很小，而NADH对硝普钠的作用可被四氮唑蓝、铁氰化铁和二苯基碘抑制。NADH氧化还原酶活性丰富的膜组分显示硝普钠释放NADH依赖的NO；硝普钠引起NADH的消耗，并抑制NADH依赖的硝基蓝四氮唑的还原。因此，膜结合的NADH氧化还原酶似乎有助于小牛肺动脉硝普钠释放NO，而不是硝酸甘油。
—The site of metabolism in vascular smooth muscle responsible for the release of nitric oxide (NO) from nitroprusside is not well established. In this study we observed that a membrane-bound NADH oxidoreductase in the pulmonary artery activates nitroprusside to release NO, and we examined whether this process could potentially participate in relaxation to nitroprusside. Relaxation to nitroprusside in bovine calf pulmonary artery is inhibited by a scavenger of NO and by an antagonist of NO stimulation of guanylate cyclase. A flavoprotein probe that inhibits pulmonary artery NADH oxidoreductase (1 μmol/L diphenyliodonium) and electron acceptors for NADH oxidoreductase (0.3 mmol/L nitroblue tetrazolium and 0.1 mmol/L ferricyanide) inhibited pulmonary artery relaxation to nitroprusside, but not to nitroglycerin. Pulmonary arteries were observed to promote the release of NO from nitroprusside in vitro, and NO release was inhibited by the presence of nitroblue tetrazolium, ferricyanide, and diphenyliodonium. In homogenates of pulmonary arteries, NADH (0.1 mmol/L) increased the release of NO from nitroprusside by ≈6-fold, whereas NADPH, mitochondrial substrates, and other redox cofactors had minimal effects on NO release, and the action of NADH on nitroprusside was inhibited by nitroblue tetrazolium, ferricyanide, and diphenyliodonium. A membrane fraction enriched in NADH oxidoreductase activity showed a NADH-dependent release of NO from nitroprusside; nitroprusside caused NADH consumption, and it also inhibited the NADH-dependent reduction of nitroblue tetrazolium. Thus, a membrane-bound NADH oxidoreductase appears to contribute to the release of NO from nitroprusside, but not nitroglycerin, in calf pulmonary artery.