中文摘要：

短暂受体潜力 Ankyrin 1 (TRPA1 ) 阳离子隧道被各种各样的刺鼻、刺激的混合物激活，并且它也调停有害寒冷的感觉。为这条隧道的不同收缩筋的鉴定为理解它的激活机制是重要的。因此，为新奇 TRPA1 收缩筋的一幅屏幕用导致收缩筋的钙流入试金被执行。从屏蔽的 90 混合物， pinacidil 为这条隧道作为新奇收缩筋被识别。Pinacidil 是 Katp 隧道，它为有 13 mol/L 的 EC50 价值的已知的启子。在比较，为 TRPA1 的 pinacidil 的 EC50 价值相对高(260 mol/L ) 。Recombinant HEK-TRPA1 房间没对 P1075 作出回应，另一 Katp 隧道启子，建议 TRPA1 上的 pinacidil 的效果是高度特定的。进一步的研究表明 pinacidil 的收缩筋活动能被 TRP 隧道禁止者，钌红和 HC-030031 堵住。用谷胱甘肽(GSH ) 和地点特定的 mutagenesis，我们证明 pinacidil 能在 TRPA1 的 N 终点由批评氨基酸 C619， C639 和 C663 的共有原子价修正激活 TRPA1。

英文摘要：

The transient receptor potential Ankyrin 1 （TRPA1） cation channel is activated by various pungent and irritant compounds, and it also mediates the perception of noxious cold. Identification of different agonists for this channel is important for understanding its activation mechanism. Therefore, a screen for novel TRPA1 agonists was performed using an agonist-induced calcium influx assay. Out of 90 compounds screened, pinacidil was identified as a novel agonist for this channel. Pinacidil is a known opener of the Katp channel, for which it has an EC50 value of 1-3 μmol/L. In comparison, the EC50 value of pinacidil for TRPAI is relatively high （260 μmol/L）. Recombinant HEK-TRPA1 cells did not respond to P1075, another Katp channel opener, suggesting that the effect of pinacidil on TRPA1 was highly specific. Further studies revealed that the agonist activity of pinacidil could be blocked by the TRP channel inhibitors, ruthenium red and HC-030031. Using glutathione （GSH） and site-specific mutagenesis, we demonstrated that pinacidil could activate TRPA1 by covalent modification of the critical amino acids C619, C639 and C663 in the N-terminus of TRPA 1.