Does elevated nitric oxide production enhance the release of prostacyclin from shear stressed aortic endothelial cells?
Does elevated nitric oxide production enhance the release of prostacyclin from shear stressed aortic endothelial cells?
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DOI：
10.1006/bbrc.1997.6548
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发表时间：
1997-04
影响因子：
3.1
通讯作者：
Weiguo Wang;Scott L. Diamond
中科院分区：
文献类型：
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作者：
Weiguo Wang;Scott L. Diamond
一氧化氮(NO)促进激动剂刺激的内皮细胞产生前列环素(PGI2)，而NO和超氧阴离子生成的过氧亚硝酸盐则激活环氧合酶。利用培养的牛主动脉内皮细胞(BAEC)暴露于25dynes/cm2的动脉层流切应力水平，验证了NO通过切应力内皮细胞介导PGI2合成增加的假说。剪切力引起NO和PGI2的大量快速爆发和持续释放，1小时的累积生成量分别是静止对照的0.0257和0.0193 ng-PGI2/cm~2-BAEC的9.96倍(n=4，p<；0.005)和9.16倍(n=3，p<；0.005)。NO合酶抑制剂N(G)-硝基-L-精氨酸甲酯(100微米，LNAME)和N(G)-硝基-L-精氨酸(10微米，LNA)分别使1小时累积NO释放量减少87.5%和65%(n=3，p<；0.02)，使PGI_2释放分别减少45%和55%(n=3，p=0.025)。在切变应激细胞中，大约一半的PGI2的增加是由于NO依赖的信号转导，这表明这两种扩张分子的血流动力学控制是部分耦合的。
Nitric oxide (NO) enhances prostacyclin (PGI2) production in agonist-stimulated endothelial cells, while peroxynitrite formed from NO and superoxide anion has been shown to activate cyclooxygenase. Using cultured bovine aortic endothelial cells (BAEC) exposed to arterial levels of laminar shear stress of 25 dynes/ cm2, we tested the hypothesis that NO mediated the elevated synthesis of PGI2 by shear stressed endothelium. Shear stress caused a large and rapid burst and sustained release of NO and PGI2 with the cumulative production at 1 hr enhanced 9.96-fold (n = 4, p < 0.005) and 9.16-fold (n = 3, p < 0.005), respectively, over stationary control production of 0.0257 nmol-NO/cm2-BAEC and 0.0193 ng-PGI2/cm2-BAEC. The NO synthase inhibitors, N(G)-nitro-L-arginine methyl ester (100 microM, LNAME) and N(G)-nitro-L-arginine (10 microM, LNA), caused 87.5 and 65% reductions (n = 3, p < 0.02) of cumulative NO release at 1 hr, respectively, and 45 and 55% reductions (n = 3, p = 0.025) of PGI2 release, respectively. About half of the elevated production of PGI2 in shear stressed cells was due to NO-dependent signaling, indicating that hemodynamic control of these two dilatory molecules is partially coupled.