Findlay I, Dunne M J
Pflugers Arch. 1986 Aug;407(2):238-40. doi: 10.1007/BF00580683.
In patch-clamp records of K+ ATP channels in an insulin-secreting cell line (RINm5F) inhibition evoked by exposing the internal surface of the membrane to ATP is followed not just by the recovery of K+ ATP channel activity when the ATP is removed but by a marked activation of K+ ATP channels. This phenomenon is not a direct consequence of channel closure as inhibition induced by quinidine and quinine is followed upon the removal of the drug only by the recovery of K+ ATP channel activity and not by post-inhibitory activation. If ATP is applied to the exposed internal surface of a membrane patch when all of its K+ ATP channel have run down subsequent removal of the ATP causes their activation. The magnitude and duration of the reactivation of K+ ATP channels is shown to depend upon both the concentration of ATP and the length of time for which the membrane is exposed to ATP. We therefore have a paradoxical situation in that K+ channels which are inhibited by intracellular ATP require intracellular ATP to retain the ability to open.
在胰岛素分泌细胞系（RINm5F）的钾离子ATP通道的膜片钳记录中，当将膜的内表面暴露于ATP引起抑制后，不仅在去除ATP时钾离子ATP通道活性会恢复，而且钾离子ATP通道会显著激活。这种现象不是通道关闭的直接结果，因为奎尼丁和奎宁诱导的抑制在去除药物后仅伴随着钾离子ATP通道活性的恢复，而没有抑制后激活。当膜片的所有钾离子ATP通道都耗尽时，如果将ATP应用于暴露的膜内表面，随后去除ATP会导致它们激活。钾离子ATP通道再激活的幅度和持续时间显示取决于ATP的浓度以及膜暴露于ATP的时间长度。因此，我们面临一种自相矛盾的情况，即被细胞内ATP抑制的钾离子通道需要细胞内ATP来保持开放能力。
