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ATP诱导的Ca2+内流导致大鼠门静脉平滑肌细胞内储存钙的释放。

Release of Ca2+ from intracellular store in smooth muscle cells of rat portal vein by ATP-induced Ca2+ entry.

作者信息

Pacaud P, Grégoire G, Loirand G

机构信息

Laboratoire de Physiologie, Faculté de médecine Victor Pachon, Université de Bordeaux II, France.

出版信息

Br J Pharmacol. 1994 Oct;113(2):457-62. doi: 10.1111/j.1476-5381.1994.tb17011.x.

Abstract
  1. The action of adenosine 5'-triphosphate (ATP, 10 microM) was studied in single patch-clamped smooth muscle cells of rat portal vein where the free internal Ca2+ concentration in the cell (Cai) was estimated by the emission from the dye indo-1. 2. In the presence of 20 microM gallopamil (D600), a blocker of voltage-dependent Ca2+ channels, ATP applied to cells held at a holding potential of -60 mV evoked a transient inward current and an increase in Cai. 3. The rise in Cai evoked by ATP was completely suppressed in the absence of external Ca2+ although a transient inward current was still observed. 4. ATP-induced responses were not modified by the addition of the inositol 1,4,5-trisphosphate receptor antagonist, heparin (1 mM) in the pipette solution. 5. In the presence of caffeine (5 mM) or ryanodine (100 microM) in the pipette solution, which deplete the intracellular Ca2+ store, the ATP-induced Cai rise was greatly reduced. 6. Our results suggest that in single cells from rat portal vein, ATP releases Ca2+ from intracellular stores without involving InsP3, but via a Ca2+ release mechanism activated by Ca2+ influx through ATP-gated channels.
摘要
  1. 在大鼠门静脉的单个膜片钳制平滑肌细胞中研究了5'-三磷酸腺苷(ATP,10微摩尔)的作用,其中细胞内游离Ca2+浓度(Cai)通过染料indo-1的荧光发射进行估算。2. 在存在20微摩尔加洛帕米(D600,一种电压依赖性Ca2+通道阻滞剂)的情况下,将ATP施加于保持在-60毫伏钳制电位的细胞时,会诱发一个短暂的内向电流和Cai的增加。3. 尽管仍观察到短暂的内向电流,但在无细胞外Ca2+时,ATP诱发的Cai升高被完全抑制。4. 在移液管溶液中添加1,4,5-三磷酸肌醇受体拮抗剂肝素(1毫摩尔)不会改变ATP诱导的反应。5. 在移液管溶液中存在咖啡因(5毫摩尔)或ryanodine(100微摩尔)(它们会耗尽细胞内Ca2+储存)时,ATP诱导的Cai升高会大大降低。6. 我们的结果表明,在大鼠门静脉的单个细胞中,ATP从细胞内储存释放Ca2+,不涉及肌醇三磷酸(InsP3),而是通过由通过ATP门控通道的Ca2+内流激活的Ca2+释放机制。

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