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

被引:1
|
作者
Park, Kyeong-Eon [1 ]
Lee, Soo Hee [2 ,3 ,6 ]
Bae, Sung Il [1 ]
Hwang, Yeran [1 ]
Ok, Seong-Ho [2 ,3 ,6 ]
Kang, Dawon [4 ]
Ahn, Seung Hyun [1 ,6 ]
Sim, Gyujin [1 ,6 ]
Park, Jin Kyeong [1 ]
Sohn, Ju-Tae [1 ,5 ,6 ]
机构
[1] Gyeongsang Natl Univ Hosp, Dept Anesthesiol & Pain Med, 79 Gangnam Ro, Jinju Si 52727, Gyeongsangnam D, South Korea
[2] Gyeongsang Natl Univ, Changwon Hosp, Dept Anesthesiol & Pain Med, Changwon Si, Gyeongsangnam D, South Korea
[3] Gyeongsang Natl Univ, Coll Med, Dept Anesthesiol & Pain Med, Jinju Si, Gyeongsangnam D, South Korea
[4] Gyeongsang Natl Univ, Coll Med, Dept Physiol, Jinju Si, Gyeongsangnam D, South Korea
[5] Gyeongsang Natl Univ, Gyeongsang Natl Univ Hosp, Coll Med, Dept Anesthesiol & Pain Med, Jinju Si, Gyeongsangnam D, South Korea
[6] Gyeongsang Natl Univ, Inst Hlth Sci, Jinju Si, Gyeongsangnam D, South Korea
基金
新加坡国家研究基金会;
关键词
KATP channel; Levcromakalim; Vasodilation; Chloroquine; Reactive oxygen; species; K+-CHANNELS; RELAXATIONS; TOXICITY; OVERDOSE; GLUCOSE; DRUGS;
D O I
10.4149/gpb_2023008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study examined the effect of chloroquine on vasodilation induced by levcromakalim in isolated endothelium-denuded rat aortas and clarified the underlying mechanisms. We exam-ined the effects of chloroquine, hydroxychloroquine, lipid emulsion, reactive oxygen species (ROS) scavenger N-acetyl-ʟ-cysteine (NAC), and KATP channel inhibitor glibenclamide on levcromakalim-induced 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 hydroxychloro-quine 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.
引用
收藏
页码:297 / 306
页数:10
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