Chloroquine inhibits vasodilation induced by ATP-sensitive potassium channels in isolated rat aorta.

IF 16.4 1区化学 Q1 CHEMISTRY, MULTIDISCIPLINARY Accounts of Chemical Research Pub Date : 2023-05-01 DOI:10.4149/gpb_2023008

Kyeong-Eon Park, Soo Hee Lee, Sung Il Bae, Yeran Hwang, Seong-Ho Ok, Dawon Kang, Seung Hyun Ahn, Gyujin Sim, Jin Kyeong Park, Ju-Tae Sohn

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Abstract

This study examined the effect of chloroquine on vasodilation induced by levcromakalim in isolated endothelium-denuded rat aortas and clarified the underlying mechanisms. We examined the effects of chloroquine, hydroxychloroquine, lipid emulsion, reactive oxygen species (ROS) scavenger N-acetyl-ʟ-cysteine (NAC), and KATP channel inhibitor glibenclamide on levcromakaliminduced vasodilation. The effects of chloroquine, hydroxychloroquine, NAC, and levcromakalim on membrane hyperpolarization and ROS production were examined in aortic vascular smooth muscle cells (VSMCs). Chloroquine inhibited levcromakalim-induced vasodilation more than hydroxychloroquine. NAC attenuated chloroquine-mediated inhibition of levcromakalim-induced vasodilation, while lipid emulsion had no effect. Glibenclamide eliminated levcromakalim-induced vasodilation in aortas pretreated with chloroquine. Chloroquine and hydroxychloroquine inhibited levcromakalim-induced membrane hyperpolarization in VSMCs. Chloroquine and hydroxychloroquine both produced ROS, but chloroquine produced more. NAC inhibited chloroquine-induced ROS production in VSMCs. Collectively, these results suggest that, partially through ROS production, chloroquine inhibits levcromakalim-induced vasodilation. In addition, chloroquine-induced KATP channel-induced vasodilation impairment was not restored by lipid emulsion.

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氯喹抑制离体大鼠主动脉atp敏感钾通道诱导的血管舒张。

本研究研究了氯喹对左旋克马卡林诱导的大鼠离体内皮剥离主动脉血管扩张的影响，并阐明了其可能的机制。我们研究了氯喹、羟氯喹、脂质乳剂、活性氧(ROS)清除剂n -乙酰基- -半胱氨酸(NAC)和KATP通道抑制剂格列本脲对左旋克罗玛alimi诱导的血管舒张的影响。研究了氯喹、羟氯喹、NAC和左旋莫卡林对主动脉血管平滑肌细胞(VSMCs)膜超极化和ROS生成的影响。氯喹比羟氯喹更能抑制左旋克马卡林诱导的血管舒张。NAC减弱了氯喹介导的左旋克罗马卡林诱导的血管舒张抑制，而脂质乳则没有作用。格列本脲消除氯喹预处理主动脉左旋克马卡林引起的血管舒张。氯喹和羟氯喹抑制左旋克马卡林诱导的VSMCs膜超极化。氯喹和羟氯喹都产生活性氧，但氯喹产生的活性氧更多。NAC抑制氯喹诱导的VSMCs ROS生成。总的来说，这些结果表明，部分通过ROS的产生，氯喹抑制左旋克罗马卡林诱导的血管舒张。此外，氯喹诱导的KATP通道诱导的血管舒张功能损伤不能通过脂质乳恢复。

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来源期刊

Accounts of Chemical Research 化学-化学综合

CiteScore

31.40

自引率

1.10%

发文量

312

审稿时长

2 months

期刊介绍： Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance. Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.

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