Sarosi G A, Barnhart D C, Turner D J, Mulholland M W
Department of Surgery, University of Michigan, Ann Arbor, Michigan 48109-0331, USA.
Am J Physiol. 1998 Sep;275(3):G550-5. doi: 10.1152/ajpgi.1998.275.3.G550.
Mobilization of intracellular Ca2+ stores is coupled to Ca2+ influx across the plasma membrane, a process termed capacitative Ca2+ entry. Capacitative Ca2+ entry was examined in cultured guinea pig enteric glia exposed to 100 microM ATP, an inositol trisphosphate-mediated Ca2+-mobilizing agonist, and to 1 microM thapsigargin, an inhibitor of microsomal Ca2+ ATPase. Both agents caused mobilization of intracellular Ca2+ stores followed by influx of extracellular Ca2+. This capacitative Ca2+ influx was inhibited by Ni2+ (88 +/- 1%) and by La3+ (87 +/- 1%) but was not affected by L- or N-type Ca2+ channel blockers. Pretreatment of glia with 100 nM phorbol 12-myristate 13-acetate for 24 h decreased capacitative Ca2+ entry by 48 +/- 2%. Chelerythrine (0.1-10 microM), a specific antagonist of protein kinase C (PKC), dose dependently inhibited capacitative Ca2+ entry. The nitric oxide synthase inhibitor NG-nitro-L-arginine (1 mM) decreased Ca2+ influx by 42 +/- 1%. Capacitative Ca2+ entry was inhibited to a similar degree by the guanylate cyclase inhibitor (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one). Capacitative Ca2+ entry occurs in enteric glial cells via lanthanum-inhibitable channels through a process regulated by PKC and nitric oxide.
细胞内钙库的动员与钙离子跨质膜内流相偶联，这一过程称为容量性钙离子内流。在培养的豚鼠肠神经胶质细胞中检测容量性钙离子内流，这些细胞暴露于100微摩尔ATP（一种肌醇三磷酸介导的钙离子动员激动剂）和1微摩尔毒胡萝卜素（一种微粒体钙ATP酶抑制剂）中。这两种试剂均引起细胞内钙库的动员，随后细胞外钙离子内流。这种容量性钙离子内流受到镍离子（88±1%）和镧离子（87±1%）的抑制，但不受L型或N型钙离子通道阻滞剂的影响。用100纳摩尔佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯预处理神经胶质细胞24小时，可使容量性钙离子内流降低48±2%。白屈菜红碱（0.1 - 10微摩尔），一种蛋白激酶C（PKC）特异性拮抗剂，剂量依赖性地抑制容量性钙离子内流。一氧化氮合酶抑制剂NG - 硝基 - L - 精氨酸（1毫摩尔）使钙离子内流降低42±1%。鸟苷酸环化酶抑制剂（1H - [1,2,4]恶二唑并[4,3 - a]喹喔啉 - 1 - 酮）对容量性钙离子内流的抑制程度相似。容量性钙离子内流通过镧离子可抑制的通道在肠神经胶质细胞中发生，该过程受PKC和一氧化氮调节。
