Wellman G C, Quayle J M, Standen N B
Ion Channel Group, Department of Cell Physiology and Pharmacology, University of Leicester, PO Box 138, Leicester LE1 9HN, UK.
Pflugers Arch. 1996 Jun;432(2):355-7. doi: 10.1007/s004240050144.
We used whole-cell patch clamp to record inward rectifier (KIR) and ATP-sensitive (KATP) K+ currents from pig coronary arterial myocytes. KIR currents were blocked by Ba2+ ions with a KD around 3 microM, but were unaffected by 10 microM glibenclamide, and only reduced 16% by 100 microM of the sulphonlyurea (n=4). In contrast, pinacidil-activated KATP currents were over 1000 times more sensitive to glibenclamide, being inhibited with a KD close to 100 nM (n=5). Our findings suggest that the sulphonylurea receptor (SUR) in these cells associates with the appropriate subunits of the Kir family to form KATP channels, but does not show promiscuous association with subunits that form the strong inward rectifier KIR.
我们采用全细胞膜片钳技术记录猪冠状动脉肌细胞的内向整流钾通道（KIR）电流和ATP敏感性钾通道（KATP）电流。KIR电流被Ba2+离子阻断，解离常数（KD）约为3微摩尔，但不受10微摩尔格列本脲的影响，仅在100微摩尔磺酰脲作用下降低16%（n = 4）。相比之下，吡那地尔激活的KATP电流对格列本脲的敏感性高1000倍以上，KD接近100纳摩尔时受到抑制（n = 5）。我们的研究结果表明，这些细胞中的磺酰脲受体（SUR）与Kir家族的相应亚基结合形成KATP通道，但不与形成强内向整流KIR的亚基发生混杂结合。
