BRADYKININ AND ATP STIMULATE L-ARGININE UPTAKE AND NITRIC-OXIDE RELEASE IN VASCULAR ENDOTHELIAL-CELLS
BRADYKININ AND ATP STIMULATE L-ARGININE UPTAKE AND NITRIC-OXIDE RELEASE IN VASCULAR ENDOTHELIAL-CELLS
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DOI：
10.1016/s0006-291x(05)81154-4
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发表时间：
1991-10-31
影响因子：
3.1
通讯作者：
MANN, GE
中科院分区：
文献类型：
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作者：
BOGLE, RG;COADE, SB;MANN, GE
在微载体上培养和灌注并缺乏 L-精氨酸 24 小时的猪主动脉内皮细胞中，研究了缓激肽和 ATP 对 L-精氨酸转运和一氧化氮 (NO) 产生的影响。用缓激肽 (100 nM) 或 ATP (100 μM) 刺激细胞会导致 L-精氨酸摄取和 NO 释放迅速增加。在 NO 合成酶抑制剂硝基-L-精氨酸 (100 μM) 存在下，缓激肽对 L-精氨酸摄取的刺激作用被部分抑制，而 NO 释放被完全消除。单独的硝基-L-精氨酸不是基础L-精氨酸转运的抑制剂，表明其抑制作用不是直接作用于L-精氨酸转运蛋白，而是抑制NO生成的结果。这些数据表明，在激动剂刺激的NO产生过程中，L-精氨酸向内皮细胞的转运同时增加，从而提供了持续产生NO的机制。
The effects of bradykinin and ATP on L-arginine transport and nitric oxide (NO) production were studied in porcine aortic endothelial cells cultured and perfused on microcarriers and deprived of L-arginine for 24 h. Stimulation of cells with bradykinin (100 nM) or ATP (100 μM) resulted in a rapid increase in L-arginine uptake and NO release. In the presence of nitro-L-arginine (100 μM), an inhibitor of NO synthase, the stimulatory effect of bradykinin on L-arginine uptake was partially inhibited while NO release was completely abolished. Nitro-L-arginine alone was not an inhibitor of basal L-arginine transport, suggesting that its inhibitory action was not directly on the L-arginine transporter but a result of the inhibition of NO generation. These data indicate that during agonist-stimulated NO production there is a concomitant increase in the transport of L-arginine into endothelial cells providing a mechanism for the continual generation of NO.