Kwak Y G, Park S K, Kim U H, Han M K, Eun J S, Cho K P, Chae S W
Department of Pharmacology, Chonbuk National University Medical School, Chonju, South Korea.
Am J Physiol. 1996 Aug;271(2 Pt 1):C464-8. doi: 10.1152/ajpcell.1996.271.2.C464.
Cyclic ADP-ribose (cADPR), an NAD metabolite, has been shown to be a messenger for Ca2+ mobilization from intracellular Ca2+ stores. However, the physiological role of ADP-ribose (ADPR), another metabolite of NAD, is not known. We examined the effects of cADPR and ADPR on the ATP-sensitive K+ channel (KATP) activity in rat ventricular myocytes by use of the inside-out patch-clamp configuration. ADPR, but not cADPR, inhibited the channel activity at micromolar range with an inhibitor constant (Ki) of 38.4 microM. The Hill coefficient was 0.9. ATP inhibited the K+ channel with a Ki of 77.8 microM, and the Hill coefficient was 1.8. Single-channel conductance was not affected by ADPR. These findings strongly suggest that ADPR may act as a regulator of KATP channel activity.
环磷酸腺苷核糖（cADPR）是一种烟酰胺腺嘌呤二核苷酸（NAD）代谢产物，已被证明是细胞内钙库释放钙离子的信使。然而，NAD的另一种代谢产物腺苷二磷酸核糖（ADPR）的生理作用尚不清楚。我们采用内面向外式膜片钳技术，研究了cADPR和ADPR对大鼠心室肌细胞中ATP敏感性钾通道（KATP）活性的影响。ADPR而非cADPR在微摩尔浓度范围内抑制通道活性，其抑制常数（Ki）为38.4微摩尔。希尔系数为0.9。ATP以77.8微摩尔的Ki抑制钾通道，希尔系数为1.8。单通道电导不受ADPR影响。这些发现强烈表明，ADPR可能作为KATP通道活性的调节剂。
