代谢抑制效果glimepiride本地块和克隆心脏sarcolemmal K (ATP)通道。

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劳伦斯CL,彩虹RD,戴维斯NW, Standen NB

代谢抑制效果glimepiride本地块和克隆心脏sarcolemmal K (ATP)通道。

Br J杂志。2002年7月,136 (5):746 - 52。

PubMed ID

12086984 (在PubMed

]

文摘

1。我们调查的影响,磺脲glimepiride,目前用于治疗2型糖尿病,ATP-sensitive K (+) (K (ATP))电流的老鼠心脏细胞,克隆成分Kir6.2和SUR2A表达HEK 293细胞。2。Glimepiride阻塞pinacidil-activated全细胞K (ATP)电流的心脏细胞IC(50)为6.8纳米,在这些细胞与格列本脲的效力。Glimepiride阻塞K (ATP)通道由co-expression Kir6.2 / SUR2A子单元HEK 293细胞外部切除补丁类似的集成电路(50)为6.2 nM。3所示。Glimepiride是更有效地阻断K (ATP)电流激活通过代谢抑制碘乙酸(MI)和CN(-)或K (ATP)通道揭幕战氯甲苯噻嗪的抑制剂的F(0)和F(1)腺苷三磷酸酶(寡霉素)和肌酸激酶(DNFB)。因此10 microM glimepiride阻塞pinacidil-activated电流> 99%,70%,diazoxide-activated MI-activated电流电流82%。4所示。从内向外补丁HEK 293细胞表达克隆的K (ATP)通道亚单位Kir6.2 / SUR2A, ADP的浓度增加(1 - 100 microM),在100海里glimepiride的存在,导致Kir6.2 / SUR2A通道活动明显增加。 However, over the range tested, ADP did not affect cloned K(ATP) channel activity in the presence of 100 nM glibenclamide. These results are consistent with the suggestion that ADP reduces glimepiride block of K(ATP) channels. 5. Our results show that glimepiride is a potent blocker of native cardiac K(ATP) channels activated by pinacidil and blocks cloned Kir6.2/SUR2A channels activated by ATP depletion with similar potency. However, glimepiride is much less effective when K(ATP) channels are activated by MI and this may reflect a reduction in glimepiride block by increased intracellular ADP.

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药物靶点

药物	目标	类	生物	药理作用	行动
Glimepiride	ATP-sensitive内向整流钾通道11	蛋白质	人类	是的	抑制剂	细节