Insulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells.
Insulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells.
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胰岛素样生长因子 I 抑制血管平滑肌细胞中一氧化氮合酶的诱导。
DOI：
10.1161/01.res.74.1.24
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发表时间：
1994
影响因子：
20.1
通讯作者：
Vanhoutte,PM
中科院分区：
文献类型：
--
作者：
Schini,VB;Catovsky,S;Schray-Utz,B;Busse,R;Vanhoutte,PM
实验旨在检查血管细胞响应损伤而产生的胰岛素样生长因子 I (IGF-I) 是否影响大鼠主动脉平滑肌细胞培养物中诱导型一氧化氮合酶诱发的一氧化氮的产生。通过测量亚硝酸盐积累和一氧化氮合酶活性（通过确定 L-精氨酸形成 L-瓜氨酸）来间接评估一氧化氮的产生。在暴露于白细胞介素 1 β (IL-1 β) 或肿瘤坏死因子 α (TNF-α) 的血管平滑肌细胞中，一氧化氮合酶被诱导。 IGF-I 以浓度依赖性方式抑制由 IL-1 β 或 TNF-α 引起的亚硝酸盐和 L-瓜氨酸的产生。 IGF-I 引起的抑制需要在一氧化氮合酶的诱导过程中生长因子的存在。两种IGF-I相关蛋白IGF-II和胰岛素也抑制IL-1β刺激的亚硝酸盐的释放和L-瓜氨酸的形成，但程度较小。在生物测定条件下，来自含有IL-1β处理的平滑肌细胞的柱的灌注液松弛了已用去氧肾上腺素收缩的无内皮的大鼠主动脉环；这些松弛被硝基-L-精氨酸逆转。将IL-1β处理的血管平滑肌细胞添加到吲哚美辛处理的血小板中可抑制它们向凝血酶的聚集；亚甲蓝阻止了这种抑制作用。对照平滑肌细胞或单独暴露于 IGF-I 的细胞没有这样的效果。（摘要截断为 250 字）
Experiments were designed to examine whether or not insulin-like growth factor I (IGF-I), which is produced by vascular cells in response to injury, affects the production of nitric oxide evoked by the inducible nitric oxide synthase in cultures of smooth muscle cells from the rat aorta. Nitric oxide production was assessed indirectly by the measurement of nitrite accumulation and nitric oxide synthase activity by determining the formation of L-citrulline from L-arginine. Nitric oxide synthase was induced in vascular smooth muscle cells that had been exposed to interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha). IGF-I inhibited, in a concentration-dependent manner, the production of nitrite and L-citrulline evoked by IL-1 beta or TNF-alpha. The inhibition caused by IGF-I required the presence of the growth factor during the induction of nitric oxide synthase. Two IGF-I-related proteins, IGF-II and insulin, also inhibited, but to a smaller extent, the release of nitrite and the formation of L-citrulline stimulated by IL-1 beta. Under bioassay conditions, the perfusates from columns containing IL-1 beta-treated smooth muscle cells relaxed rings of rat aorta without endothelium that had been contracted with phenylephrine; these relaxations were reversed by nitro-L-arginine. Addition of IL-1 beta-treated vascular smooth muscle cells to indomethacin-treated platelets inhibited their aggregation to thrombin; methylene blue prevented this inhibition. Control smooth muscle cells or cells exposed to IGF-I alone did not have such effects.(ABSTRACT TRUNCATED AT 250 WORDS)