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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Mepivacaine attenuates vasodilation induced by ATP-sensitive potassium channels in rat aorta
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Mepivacaine attenuates vasodilation induced by ATP-sensitive potassium channels in rat aorta

机译：甲哌卡因可减轻ATP敏感性钾通道在大鼠主动脉中引起的血管舒张作用

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摘要

The goal of this in vitro study was to investigate the effect of mepivacaine on vasodilation induced by the ATP-sensitive potassium (K-ATP) channel opener levcromakalim in isolated endothelium-denuded rat aortas. The effects of mepivacaine and the K-ATP channel inhibitor glibenclamide, alone or in combination, on levcromakalim-induced vasodilation were assessed in the isolated aortas. The effects of mepivacaine or combined treatment with a protein kinase C (PKC) inhibitor, GF109203X, and mepivacaine on this vasodilation were also investigated. Levcromakalim concentration-response curves were generated for isolated aortas precontracted with phenylephrine or a PKC activator, phorbol 12,13-dibutyrate (PDBu). Further, the effects of mepivacaine and glibenclamide on levcromakalim-induced hyperpolarization were assessed in rat aortic vascular smooth muscle cells. Mepivacaine attenuated levcromakalim-induced vasodilation, whereas it had no effect on this vasodilation in isolated aortas pretreated with glibenclamide. Combined treatment with GF109203X and mepivacaine enhanced levcromakalim-induced vasodilation compared with pretreatment with mepivacaine alone. This vasodilation was attenuated in aortas precontracted with PDBu compared with those precontracted with phenylephrine. Mepivacaine and glibenclamide, alone or in combination, attenuated levcromakalim-induced membrane hyperpolarization. Taken together, these results suggest that mepivacaine attenuates vasodilation induced by K-ATP channels, which appears to be partly mediated by PKC.
机译：这项体外研究的目的是研究甲哌卡因对ATP敏感性钾（K-ATP）通道开放剂levcromakalim在分离的内皮剥夺的大鼠主动脉中诱导的血管舒张作用。在分离的主动脉中评估了甲哌卡因和K-ATP通道抑制剂格列本脲单独或联合使用对左克罗姆卡林诱导的血管舒张的作用。还研究了甲哌卡因或与蛋白激酶C（PKC）抑制剂GF109203X和甲哌卡因联合治疗对这种血管舒张作用的影响。对于与苯肾上腺素或PKC活化剂佛波醇12,13-二丁酸酯（PDBu）预缩合的离体主动脉，生成了左氯卡莫林的浓度-响应曲线。此外，在大鼠主动脉血管平滑肌细胞中评估了甲哌卡因和格列本脲对左旋卡马林诱导的超极化的影响。甲哌卡因减弱了左克cromakalim诱导的血管舒张作用，而在使用格列本脲预处理的离体主动脉中，它对这种血管舒张作用没有影响。与单独使用甲哌卡因预处理相比，用GF109203X和甲哌卡因联合治疗可增强左卡罗卡林诱导的血管舒张作用。与用苯肾上腺素预收缩的患者相比，用PDBu预收缩的主动脉的这种血管舒张作用减弱。甲哌卡因和格列本脲单独或联合使用可减轻左克罗姆卡林诱导的膜超极化。两者合计，这些结果表明，甲哌卡因减弱了由K-ATP通道诱导的血管舒张作用，后者似乎部分由PKC介导。

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