Gagov H S, Duridanova D B, Boev K K, Daniel E E
Institute of Physiology, Bulgarian Academy of Sciences, Sofia.
Gen Physiol Biophys. 1994 Apr;13(2):75-84.
The relationship between inositol-1,4,5-trisphosphate-sensitive Ca2+ stores and Ca2+ entry through potential-dependent L-type Ca2+ channels was examined using whole-cell voltage-clamp technique in cells of longitudinal muscle layer of guinea-pig ileum. It was found that heparin (10(-10) mol/l) in the pipette rapidly inhibited the current through L-type Ca2+ channels. Neither an inhibitor of the sarcoplasmic reticulum Ca2+ pump (cyclopiazonic acid) nor blockers of Ca(2+)-induced Ca2+ release (ryanodine or ruthenium red) affected the Ca2+ current. The failure of heparin to affect Ca(2+)-currents through L-type Ca2+ channels in cells from circular muscle of the same organ suggested that heparin had no direct effect on L-type Ca2+ channels. Thus the inhibition of the latter in heparin-loaded cells from the longitudinal layer is supposed to be Ca(2+)-dependent due to the overfilling of the inositol-1,4,5-trisphosphate-sensitive Ca2+ store.
采用全细胞膜片钳技术,在豚鼠回肠纵肌层细胞中研究了肌醇-1,4,5-三磷酸敏感的钙库与通过电压依赖性L型钙通道的钙内流之间的关系。发现移液管中的肝素(10⁻¹⁰mol/L)迅速抑制通过L型钙通道的电流。肌浆网钙泵抑制剂(环匹阿尼酸)和钙诱导的钙释放阻滞剂(ryanodine或钌红)均不影响钙电流。肝素对同一器官环肌细胞中通过L型钙通道的钙电流无影响,提示肝素对L型钙通道无直接作用。因此,由于肌醇-1,4,5-三磷酸敏感的钙库过度充盈,肝素处理的纵肌层细胞中L型钙通道的抑制被认为是钙依赖性的。