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丙泊酚和硫喷妥钠对肌膜三磷酸腺苷敏感性钾通道抑制作用的分子机制

Molecular mechanisms of the inhibitory effects of propofol and thiamylal on sarcolemmal adenosine triphosphate-sensitive potassium channels.

作者信息

Kawano Takashi, Oshita Shuzo, Takahashi Akira, Tsutsumi Yasuo, Tomiyama Yoshinobu, Kitahata Hiroshi, Kuroda Yasuhiro, Nakaya Yutaka

机构信息

Department of Anesthesiology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima 770-8503, Japan.

出版信息

Anesthesiology. 2004 Feb;100(2):338-46. doi: 10.1097/00000542-200402000-00024.

Abstract

BACKGROUND

Both propofol and thiamylal inhibit adenosine triphosphate-sensitive potassium (KATP) channels. In the current study, the authors investigated the effects of these anesthetics on the activity of recombinant sarcolemmal KATP channels encoded by inwardly rectifying potassium channel (Kir6.1 or Kir6.2) genes and sulfonylurea receptor (SUR1, SUR2A, or SUR2B) genes.

METHODS

The authors used inside-out patch clamp configurations to investigate the effects of propofol and thiamylal on the activity of recombinant KATP channels using COS-7 cells transfected with various types of KATP channel subunits.

RESULTS

Propofol inhibited the activities of the SUR1/Kir6.2 (EC50 = 77 microm), SUR2A/Kir6.2 (EC50 = 72 microm), and SUR2B/Kir6.2 (EC50 = 71 microm) channels but had no significant effects on the SUR2B/Kir6.1 channels. Propofol inhibited the truncated isoform of Kir6.2 (Kir6.2DeltaC36) channels (EC50 = 78 microm) that can form functional KATP channels in the absence of SUR molecules. Furthermore, the authors identified two distinct mutations R31E (arginine residue at position 31 to glutamic acid) and K185Q (lysine residue at position 185 to glutamine) of the Kir6.2DeltaC36 channel that significantly reduce the inhibition of propofol. In contrast, thiamylal inhibited the SUR1/Kir6.2 (EC50 = 541 microm), SUR2A/Kir6.2 (EC50 = 248 microm), SUR2B/Kir6.2 (EC50 = 183 microm), SUR2B/Kir6.1 (EC50 = 170 microm), and Kir6.2DeltaC36 channels (EC50 = 719 microm). None of the mutants significantly affects the sensitivity of thiamylal.

CONCLUSIONS

These results suggest that the major effects of both propofol and thiamylal on KATP channel activity are mediated via the Kir6.2 subunit. Site-directed mutagenesis study suggests that propofol and thiamylal may influence Kir6.2 activity by different molecular mechanisms; in thiamylal, the SUR subunit seems to modulate anesthetic sensitivity.

摘要

背景

丙泊酚和硫喷妥钠均可抑制三磷酸腺苷敏感性钾(KATP)通道。在本研究中,作者研究了这些麻醉药对由内向整流钾通道(Kir6.1或Kir6.2)基因和磺脲类受体(SUR1、SUR2A或SUR2B)基因编码的重组肌膜KATP通道活性的影响。

方法

作者采用内面向外膜片钳配置,利用转染了各种类型KATP通道亚基的COS-7细胞,研究丙泊酚和硫喷妥钠对重组KATP通道活性的影响。

结果

丙泊酚抑制SUR1/Kir6.2(半数有效浓度[EC50]=77微摩尔)、SUR2A/Kir6.2(EC50=72微摩尔)和SUR2B/Kir6.2(EC50=71微摩尔)通道的活性,但对SUR2B/Kir6.1通道无显著影响。丙泊酚抑制了Kir6.2的截短异构体(Kir6.2DeltaC36)通道(EC50=78微摩尔),该通道在无SUR分子时可形成功能性KATP通道。此外,作者鉴定出Kir6.2DeltaC36通道的两个不同突变R31E(第31位精氨酸残基突变为谷氨酸)和K185Q(第185位赖氨酸残基突变为谷氨酰胺),它们可显著降低丙泊酚的抑制作用。相比之下,硫喷妥钠抑制SUR1/Kir6.2(EC50=541微摩尔)、SUR2A/Kir6.2(EC50=248微摩尔)、SUR2B/Kir6.2(EC50=183微摩尔)、SUR2B/Kir6.1(EC50=170微摩尔)和Kir6.2DeltaC36通道(EC50=719微摩尔)。这些突变体均未显著影响硫喷妥钠的敏感性。

结论

这些结果表明,丙泊酚和硫喷妥钠对KATP通道活性的主要影响均通过Kir6.2亚基介导。定点诱变研究表明,丙泊酚和硫喷妥钠可能通过不同的分子机制影响Kir6.2的活性;在硫喷妥钠中,SUR亚基似乎可调节麻醉药敏感性。

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