Distribution of NOS in normoxic vs. hypoxic rat lung: upregulation of NOS by chronic hypoxia.
Distribution of NOS in normoxic vs. hypoxic rat lung: upregulation of NOS by chronic hypoxia.
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NOS 在常氧与缺氧大鼠肺中的分布：慢性缺氧对 NOS 的上调。
DOI：
10.1152/ajplung.1994.267.6.l667
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Johns,RA
中科院分区：
文献类型：
--
作者：
Xue,C;Rengasamy,A;LeCras,TD;Koberna,PA;Dailey,GC;Johns,RA
应用免疫组织化学和NADPH黄递酶(NADPH-d)染色技术，对慢性低氧和正常大鼠肺组织一氧化氮合酶(NOS)的表达和定位进行了研究。常氧组和缺氧组大鼠肺大血管内皮细胞、细支气管壁和细支气管壁上皮细胞均有一氧化氮合酶表达。常氧肺阻力血管内皮细胞未见一氧化氮合酶表达，慢性低氧2~4wk时，这些血管内皮细胞有明显表达。与小肺血管不同，常氧肺和低氧肺小支气管血管内皮细胞均呈NOS免疫反应阳性。低氧还可诱导大、小肺血管和支气管平滑肌中新生一氧化氮合酶的表达。肺组织匀浆中一氧化氮合酶活性的测定采用[~3H]精氨酸-[~3H]瓜氨酸转化率法。低氧肺组织中可溶性一氧化氮合酶活性升高，而颗粒型一氧化氮合酶活性无明显变化。这些结果表明，慢性低氧诱导大鼠肺组织一氧化氮合酶蛋白表达和活性上调，提示一氧化氮在肺循环对慢性低氧的适应中可能起着重要作用。在小的肺阻力血管中缺乏免疫染色也与生理研究一致，表明NO可能不参与维持正常低肺血管阻力的机制。
Expression and localization of nitric oxide synthase (NOS) in the lungs of chronically hypoxic and normoxic rats were studied using both immunohistochemistry and NADPH diaphorase (NADPH-d) staining techniques. In the normoxic and in the hypoxic rat, NOS was detected by both methods in the endothelium of large pulmonary vessels and in the epithelium of bronchi and bronchioli. NOS expression was not detected in the endothelium of normoxic pulmonary resistance vessels but was prominently expressed in the endothelium of these vessels after 2-4 wk of chronic hypoxia. In contrast to small pulmonary vessels, the endothelium of small bronchial vessels exhibited NOS immunostaining in both normoxic and hypoxic lungs. Hypoxia was also found to induce de novo NOS expression in the smooth muscle of large and small pulmonary vessels and in bronchial smooth muscle. NOS enzyme activity in lung homogenates was assessed by [3H]arginine to [3H]citrulline conversion. The activity of soluble NOS, but not particulate NOS, was increased in the hypoxic lungs. These results demonstrate chronic hypoxia-induced upregulation of NOS protein expression and activity in the rat lung, suggesting a potentially important role of nitric oxide in adaptation of the pulmonary circulation to chronic hypoxia. The lack of immunostaining in small pulmonary resistance vessels is also consistent with physiological studies suggesting that NO may not be involved in the mechanism for maintaining the normally low pulmonary vascular resistance.