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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Elevated glucose attenuates agonist- and flow-stimulated endothelial nitric oxide synthase activity in microvascular retinal endothelial cells.
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Elevated glucose attenuates agonist- and flow-stimulated endothelial nitric oxide synthase activity in microvascular retinal endothelial cells.

机译：升高的葡萄糖减弱了微血管视网膜内皮细胞中激动剂和血流刺激的内皮一氧化氮合酶的活性。

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摘要

Impaired vasoactive release of opposing vasodilator and vasoconstrictor mediators due to endothelial dysfunction is integral to the pathogenesis of diabetic retinopathy. The aim of this study was to determine the effect of hyperglycemia on the expression of endothelial nitric oxide synthase (eNOS) and the release of nitric oxide (NO) in bovine microvascular retinal endothelial cells (BRECs) under both static (basal and acetylcholine stimulated) and flow (laminar shear stress [10 dynes/cm2 and pulsatile flow 0.3 to 23 dynes/cm2) conditions using a laminar shear apparatus and an in vitro perfused transcapillary culture system. The activity and expression of eNOS, measured by nitrate levels and immunoblot, respectively, were determined following exposure of BRECs to varying concentrations of glucose and mannitol (0 to 25 mM). Under static conditions the expression of eNOS decreased significantly following exposure to increasing concentrations of glucose when compared to osmotic mannitol controls and was accompanied by a significant dose-dependent decrease in nitrate levels in conditioned medium. The acetylcholine stimulated increase in NO release (2.0 +/- 0.3-fold) was significantly reduced by 55% +/- 5% and 65% +/- 4.5% following exposure to 16 and 25 mM glucose, respectively, when compared to osmotic controls. In parallel studies, glucose significantly inhibited both laminar shear stress and pulsatile flow-induced activity when compared to mannitol. We conclude that hyperglycemia impairs agonist- and flow-dependent release of NO in retinal microvascular endothelial cells and may thus contribute to the vascular endothelial dysfunction and impaired autoregulation of diabetic retinopathy.
机译：糖尿病性视网膜病的发病机制必不可少的是内皮功能障碍导致对立的血管扩张药和血管收缩药介导的血管活性释放受损。这项研究的目的是确定高血糖对静态（基础和乙酰胆碱刺激）下牛微血管视网膜内皮细胞（BRECs）中内皮型一氧化氮合酶（eNOS）表达和一氧化氮（NO）释放的影响使用层流剪切设备和体外灌流式毛细血管培养系统的流量和流量（层流剪切应力[10达因/平方厘米和脉动流0.3至23达因/平方厘米）条件。 BRECs暴露于不同浓度的葡萄糖和甘露醇（0至25 mM）后，分别通过硝酸盐水平和免疫印迹测定eNOS的活性和表达。与渗透性甘露醇对照相比，在静态条件下，暴露于增加浓度的葡萄糖后，eNOS的表达显着降低，并伴随着条件培养基中硝酸盐水平的剂量依赖性显着降低。与渗透压相比，分别暴露于16 mM和25 mM葡萄糖后，乙酰胆碱刺激的NO释放增加（2.0 +/- 0.3倍）显着降低了55％+/- 5％和65％+/- 4.5％。控件。在平行研究中，与甘露醇相比，葡萄糖显着抑制层流切应力和脉动血流诱导的活性。我们得出的结论是，高血糖会损害视网膜微血管内皮细胞中激动剂和血流依赖性NO的释放，因此可能导致血管内皮功能障碍和糖尿病性视网膜病变的自动调节受损。

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