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首页> 外文期刊>American Journal of Physiology >Glucose dilates renal afferent arterioles via glucose transporter-1
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Glucose dilates renal afferent arterioles via glucose transporter-1

机译：葡萄糖通过葡萄糖转运蛋白-1扩张肾传入动脉杆菌

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摘要

Glomerular hyperfiltralion occurs during the early stage of diabetes. An acute glucose infusion increases glomerular filtration rate. The involvement of tubuloglomerular feedback response and direct effect of glucose on the afferent arterioles (Af-Arts) have been suggested. However, the signaling pathways to trigger Af-Art dilatation have not been fully identified. Therefore, in the present study we tested our hypothesis that an increase in glucose concentration enhances endothelial nitric oxide synthesis activity and dilates the Af-Arts via glucose transporter-1 (GLUT1) using isolated mouse Af-Arts with perfusion. We isolated and microperfused the Af-Arts from nondiabetic C57BL/6 mice. The Af-Arts were preconstricted with norepinephrine (1μM). When we switched the D-glucose concentration from low (5 mM) to high (30 mM) in the perfusate, the preconstricted Af-Arts significantly dilated by 37.8 ± 7.1%, but L-glucose did not trigger the dilation. GLLJT1 mRNA was identified in microdisserted Af-Arts measured by RT-PCR. Changes in nitric oxide (NO) production in Af-Art were also measured using fluorescent probe when ambient glucose concentration was increased. When the D-glucose concentration was switched from 5 to 30 mM, NO generation in Af-Art was significantly increased by 19.2 ± 6.2% (84.7 ± 4.1 to 101.0 ± 9.3 U/min). L-Glucosehad no effect on the NO generation. The GLUTl-selective antagonist 4-[({[4-(1, 1 -Dimethylethyl) phenyl]sulfonyl) amino)methyl]-N-3-pyri-dinylbenzamide and the nitric oxide synthase inhibitor N~G-nitro-L-arginine methyl ester blocked the high glucose-induced NO generation and vasodilalion. In conclusion, we demonstrated that an increase in glucose concentration dilates the Af-Art by stimulation of the endothelium-derived NO production mediated by GLUT1.
机译：在糖尿病的早期阶段发生肾小球血管特拉敏。急性葡萄糖输注增加了肾小球过滤速率。已经提出了对小管状反馈反应和葡萄糖对传入动脉（AF-ARTS）的直接效应的参与。然而，尚未完全识别出触发AF-艺术扩张的信号传导途径。因此，在本研究中，我们测试了我们的假设，即葡萄糖浓度的增加增强了内皮型一氧化氮合成活性，并通过血糖转运蛋白-1（Glut1）利用灌注的分离的小鼠AF-ART来扩张AF-ARTS。我们分离和微射过来自非脂C57BL / 6小鼠的AF-ARF。 AF-ARTS用NorePinephrine（1μM）预先标记。当我们将D-葡萄糖浓度从低（5mm）切换到灌注液中的高（30毫米）时，预先预先的AF-ART显着扩张37.8±7.1％，但L-葡萄糖没有引发扩张。通过RT-PCR测量的微体AF-ART中鉴定GLLJT1 mRNA。当环境葡萄糖浓度增加时，还使用荧光探针测量AF-ART的一氧化氮（NO）产生的变化。当D-葡萄糖浓度从5〜30mm切换时，AF-ART的发电明显增加19.2±6.2％（84.7±4.1至101.0±9.3 U / min）。 L-glucosehad对不代的产生没有影响。谷蛋白选择性拮抗剂4 - [（[4-（1,1-二甲基乙基）苯基]亚磺酰基）氨基）甲基] -N-3-Pyri-列酰胺和一氧化氮合酶抑制剂N〜G-Nitro-L-精氨酸甲酯阻断了高葡萄糖诱导的不产生和血管缩水。总之，我们证明葡萄糖浓度的增加通过刺激内皮衍生的NO生产的NO生产来扩张AF-ART。

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