SUPEROXIDE ANION IS AN ENDOTHELIUM-DERIVED CONTRACTING FACTOR
SUPEROXIDE ANION IS AN ENDOTHELIUM-DERIVED CONTRACTING FACTOR
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DOI：
10.1152/ajpheart.1989.257.1.h33
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发表时间：
1989-07-01
影响因子：
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通讯作者：
VANHOUTTE, PM
中科院分区：
文献类型：
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作者：
KATUSIC, ZS;VANHOUTTE, PM
钙离子载体A23187引起犬基底动脉内皮依赖性收缩。去除内皮，或治疗与吲哚美辛或超氧化物歧化酶（SOD），防止内皮依赖性兴奋作用的钙离子载体。过氧化氢酶和去铁胺没有影响。在过氧化氢酶存在下，黄嘌呤加黄嘌呤氧化酶产生的超氧阴离子引起血管平滑肌收缩，这被SOD或黄嘌呤氧化酶的热失活所消除。A23187诱导的拟南芥素F2 α的产生。E2和血栓素B2被取消的内皮细胞和消炎痛治疗，但不受SOD加过氧化氢酶的存在。这些观察结果是一致的假设，超氧阴离子，而不是由环氧合酶的过氧化氢酶活性产生的胰头素，是犬脑动脉内皮源性收缩因子。
The calcium ionophore A23187 causes endothelium-dependent contractions in canine basilar arteries. Removal of the endothelium, or treatment with indomethacin or superoxide dismutase (SOD), prevented the endothelium-dependent excitatory effect of the calcium ionophore. Catalase and deferoxamine were without effect. Superoxide anion generated by xanthine plus xanthine oxidase in the presence of catalase caused contractions of the vascular smooth muscle, which were abolished by SOD or heat inactivation of xanthine oxidase. The A23187-induced production of prostaglandins F2.alpha. and E2 and thromboxane B2 was abolished by the removal of endothelium and by treatment with indomethacin but was not affected by the presence of SOD plus catalase. These observations are consistent with the hypothesis that superoxide anion, rather than prostaglandins generated by hydroperoxidase activity of cyclooxygenase, is an endothelium-derived contracting factor in canine cerebral arteries.