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目的 研究不同浓度胰岛素、葡萄糖对培养血管内皮细胞一氧化氮 (NO)产生的影响 ,探讨糖尿病时内皮依赖性血管舒张异常的作用机制。方法 用放免法测定内皮细胞cGMP水平来反映NO的量 ;半定量RT PCR检测NO合酶 (eNOS)mRNA水平。结果 胰岛素 (0 .18～ 6 .0nmol/L)、葡萄糖 (2 0mmol/L ,40mmol/L)能增加内皮细胞cGMP产量 ,并呈浓度和时间依赖性 ;高浓度葡萄糖上调eNOSmRNA水平 ,而胰岛素对其无影响 ;在高浓度葡萄糖下 ,胰岛素 (6 .0nmol/L)刺激NO的生成作用明显降低。结论 胰岛素介导的内皮依赖性血管扩张与胰岛素刺激内皮细胞NO合成有关 ;血管内皮对胰岛素的敏感性减低是胰岛素抵抗的一部分 ;高浓度葡萄糖可能会抑制胰岛素介导的内皮依赖性血管舒张。
Objective To study the effects of different concentrations of insulin and glucose on the production of nitric oxide (NO) in cultured vascular endothelial cells and to explore the mechanism of endothelium-dependent vasodilation in diabetic patients. Methods The levels of cGMP in endothelial cells were measured by radioimmunoassay. The levels of NO synthase (eNOS) mRNA were detected by semi-quantitative RT-PCR. Results Insulin (0.18 ~ 6.0 nmol / L) and glucose (20 mmol / L, 40 mmol / L) increased the cGMP production in endothelial cells in a dose- and time-dependent manner. Glucose upregulated eNOS mRNA expression, while insulin Its no effect; in high concentrations of glucose, insulin (6 .0nmol / L) to stimulate the production of NO was significantly reduced. Conclusion Insulin-mediated endothelium-dependent vasodilatation is associated with insulin-stimulated endothelial nitric oxide synthase (NO) synthesis. Decreased sensitivity of vascular endothelium to insulin is part of insulin resistance. High concentrations of glucose may inhibit insulin-mediated endothelium-dependent vasodilatation.