[Exogenous nitric oxide suppresses K _ATP channel activity through S-nitrosylation].

Q4 Medicine

生物医学工程学杂志 Pub Date : 2026-04-25 DOI:10.7507/1001-5515.202511038

Xuefei Wang, Yuxin Zhang, Weicao Hu, Xuewei Hao

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Abstract

The inhibitory effect of exogenous nitric oxide (NO) on the open state of ATP-sensitive potassium channels (K _ATP) and its underlying mechanism remain unclear. In this study, patch-clamp and molecular biology techniques are used to investigate this issue. In acutely isolated rat mesenteric artery smooth muscle cells and human embryonic kidney 293 cells (HEK293) expressing inwardly rectifying potassium channel 6.1 subunit/sulfonylurea receptor 2B subunit (Kir6.1/SUR2B), sodium nitroprusside (SNP) was found to significantly inhibit the activity of open K _ATP channels. Detection using biotin-labeled glutathione ethyl ester (BioGEE) combined with Western blotting showed that Kir6.1 subunit glutathionylation level was significantly decreased after SNP treatment. These results indicate that exogenous NO directly inhibits the activity of open K _ATP channels by nitrosylating key cysteine residues of the Kir6.1 subunit and competitively inhibiting glutathionylation at this site. This study provides new experimental evidence for the molecular mechanism of NO in vascular regulation.

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[外源性一氧化氮通过s -亚硝基化抑制K ATP通道活性]。

外源性一氧化氮（NO）对ATP敏感钾通道（K - ATP）开放状态的抑制作用及其机制尚不清楚。本研究采用膜片钳和分子生物学技术来研究这一问题。在急性分离的大鼠肠系膜动脉平滑肌细胞和人胚胎肾293细胞（HEK293）中，表达向内纠正钾通道6.1亚基/磺酰脲受体2B亚基（Kir6.1/SUR2B），发现硝普钠（SNP）显著抑制开放K ATP通道的活性。生物素标记谷胱甘肽乙酯（BioGEE）结合Western blotting检测显示，SNP处理后，Kir6.1亚基谷胱甘肽化水平显著降低。这些结果表明，外源NO通过亚硝基化Kir6.1亚基的关键半胱氨酸残基并竞争性地抑制该位点的谷胱甘肽化，直接抑制开放K ATP通道的活性。本研究为一氧化氮参与血管调节的分子机制提供了新的实验依据。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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