Insulin like growth factor 1 increases vascular smooth muscle nitric oxide production
Insulin like growth factor 1 increases vascular smooth muscle nitric oxide production
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DOI：
10.1016/s0024-3205(97)00594-8
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发表时间：
1997-07-25
期刊：
影响因子：
6.1
通讯作者：
Sowers, JR
中科院分区：
文献类型：
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作者：
Muniyappa, R;Walsh, MF;Sowers, JR
胰岛素样生长因子1（IGF-1）血管扩张，增加血流量和降低血压;一氧化氮（NO）已被建议介导这些作用中的一些。我们研究了IGF-1在调节血管平滑肌细胞（VSMC）NO生成中的作用。IGF-1诱导内皮剥脱的主动脉环释放NO的浓度和时间依赖性增加。用放线菌酮或氨基胍预孵育阻断IGF-1刺激的NO释放。此外，在与IGF-1孵育后，观察到VSMC产生的NO增加6倍。这些结果表明，IGF-1通过一个过程，涉及新的蛋白质合成和诱导型一氧化氮合酶亚型诱导血管平滑肌细胞NO的释放。
Insulin like growth factor 1 (IGF-1) vasodilates, increases blood flow and lowers blood pressure; nitric oxide (NO) has been suggested to mediate some of these effects. We studied the role of IGF-1 in the regulation of NO production in vascular smooth muscle cells (VSMC). IGF-1 induced a concentration and time-dependent increase in NO release from endothelium-denuded aortic rings. Pre-incubation with cycloheximide or aminoguanidine blocked IGF-l-stimulated NO release. In addition, a six-fold increase in NO production by VSMC was seen upon incubation with IGF-1. These results suggest that IGF-1 induces NO release in VSMC through a process that involves new protein synthesis and the inducible isoform of nitric oxide synthase.