Katusic Z S, Vanhoutte P M
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.
Am J Physiol. 1989 Jul;257(1 Pt 2):H33-7. doi: 10.1152/ajpheart.1989.257.1.H33.
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.
钙离子载体A23187可引起犬基底动脉的内皮依赖性收缩。去除内皮,或用吲哚美辛或超氧化物歧化酶(SOD)处理,可防止钙离子载体的内皮依赖性兴奋作用。过氧化氢酶和去铁胺无效。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,SOD或黄嘌呤氧化酶热失活可消除这种收缩。去除内皮并用吲哚美辛处理可消除A23187诱导的前列腺素F2α、E2和血栓素B2的产生,但不受SOD加过氧化氢酶存在的影响。这些观察结果与以下假设一致,即超氧阴离子而非环氧化酶的氢过氧化物酶活性产生的前列腺素是犬脑动脉中一种内皮源性收缩因子。