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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Possible involvement of potassium channels in peripheral antinociception induced by metamizol: lack of participation of ATP-sensitive K(+) channels.
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Possible involvement of potassium channels in peripheral antinociception induced by metamizol: lack of participation of ATP-sensitive K(+) channels.

机译：钾通道可能参与美他唑诱导的外周镇痛作用：缺乏ATP敏感性K（+）通道的参与。

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摘要

The present work assessed the possible participation of K(+) channels in the peripheral antinociceptive action of metamizol in the 1% formalin test. Ipsilateral, but not contralateral, local peripheral administration of metamizol produced a dose-dependent antinociception only during the second phase of the formalin test. K(+) channel blockers alone did not modify formalin-induced nociceptive behavior. However, local peripheral pretreatment of the paw with charybdotoxin and apamin (large- and small-conductance Ca(2+)-activated K(+) channel blockers, respectively), 4-aminopyridine and tetraethylammonium (voltage-dependent K(+) channel inhibitors), but not glibenclamide or tolbutamide (ATP-sensitive K(+) channel inhibitors), dose-dependently prevented metamizol-induced antinociception. The above results suggest that metamizol could open large- and small-conductance Ca(2+)-activated K(+) channels, but not ATP-sensitive K(+) channels, in order to produce its peripheral antinociceptive effect in the formalintest. The participation of voltage-dependent K(+) channels was also suggested, but since nonselective inhibitors were used, the data await further confirmation.
机译：本工作评估了在1％福尔马林测试中K（+）通道可能参与美他唑的外周镇痛作用。仅在福尔马林测试的第二阶段，美他唑的同侧而非对侧局部外周给药才产生剂量依赖性抗伤害感受。单独的K（+）通道阻滞剂不会修改福尔马林诱导的伤害行为。但是，用Charybdotoxin和apamin（分别用大和小电导Ca（2+）激活的K（+）通道阻滞剂），4-氨基吡啶和四乙铵（电压依赖的K（+）通道）进行局部外周足爪预处理抑制剂），但不是格列本脲或甲苯磺丁酰胺（ATP敏感的K（+）通道抑制剂），剂量依赖性地预防了美他唑诱导的镇痛作用。以上结果表明，美他唑可以打开大和小电导Ca（2+）激活的K（+）通道，但不能打开ATP敏感的K（+）通道，以便在形式试验中产生其外周镇痛作用。还提出了电压依赖性K（+）通道的参与，但由于使用了非选择性抑制剂，因此有待进一步证实。

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