Hisada T, Kurachi Y, Sugimoto T
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Pflugers Arch. 1990 Apr;416(1-2):151-61. doi: 10.1007/BF00370237.
Tracheal smooth muscle cells were enzymatically isolated from guinea-pig trachea. These cells contracted in response to acetylcholine (0.01-10 microM) in a concentration-dependent fashion. Under current-clamp conditions with 140 mM K+ in the pipette solution, the membrane potential oscillated spontaneously at around -30 mV. Under voltage-clamp conditions, there appeared spontaneous but steady oscillations of outward current (IO). On depolarization from a holding potential at -40 mV, three components of outward current were elicited: transient outward current (IT), steady-state outward current (IS) and IO. These three components of outward current reversed around the K+ equilibrium potential and were abolished by Cs+ in the pipette, indicating that K+ was the major charge carrier of these outward currents. All these three components were completely suppressed by extracellular tetraethylammonium (10 mM). Both IT and IO were depressed by quinidine (1 mM), 4-aminopyridine (10 mM) and nifedipine (100 nM), but IS was not affected. IT and IO were suppressed by a Ca2(+)-free perfusate with less than 1 nM Ca2+ in the pipette, while with 10 nM Ca2+ in the pipette, only IO was suppressed. In both conditions, IS was not affected by the Ca2(+)-free perfusate. Therefore, it is suggested that IO, IT and IS are separate types of K+ current. With Cs+ in the pipette, K+ currents were almost completely suppressed and a transient inward current was observed during depolarizing pulses. The inward current was not affected by tetrodotoxin and increased when the concentration of extracellular Ca2+ was raised, indicating that the current is a Ca2+ channel current. Even with a holding potential of -80 mV, the low-threshold inward current could not be observed. The high-threshold Ca2+ current was abolished by nifedipine (100 nM) and was enhanced by Bay K 8644 (100 nM). The order of permeation of divalent cations through the Ca2+ channel was Ba2+ greater than Sr2+ approximately Ca2+. Cd2+ blocked the Ca2+ current more effectively than Ni2+. These results may indicate that the Ca2+ current of tracheal smooth muscle cells is mainly composed of the current through an L-type Ca2+ channel.
气管平滑肌细胞是从豚鼠气管中通过酶法分离得到的。这些细胞对乙酰胆碱(0.01 - 10微摩尔)呈浓度依赖性收缩反应。在移液管溶液中含140毫摩尔钾离子的电流钳制条件下,膜电位在约 -30毫伏处自发振荡。在电压钳制条件下,出现了外向电流(IO)的自发但稳定的振荡。从 -40毫伏的保持电位去极化时,引发了外向电流的三个成分:瞬时外向电流(IT)、稳态外向电流(IS)和IO。外向电流的这三个成分在钾离子平衡电位附近反转,并被移液管中的铯离子消除,表明钾离子是这些外向电流的主要电荷载体。这三个成分都被细胞外四乙铵(10毫摩尔)完全抑制。IT和IO都被奎尼丁(1毫摩尔)、4 - 氨基吡啶(10毫摩尔)和硝苯地平(100纳摩尔)抑制,但IS不受影响。IT和IO被移液管中钙离子浓度低于1纳摩尔的无钙灌流液抑制,而移液管中钙离子浓度为10纳摩尔时,只有IO被抑制。在这两种情况下,IS都不受无钙灌流液的影响。因此,提示IO、IT和IS是不同类型的钾电流。移液管中加入铯离子时,钾电流几乎完全被抑制,在去极化脉冲期间观察到一个瞬时内向电流。内向电流不受河豚毒素影响,并且当细胞外钙离子浓度升高时增加,表明该电流是一种钙通道电流。即使保持电位为 -80毫伏,也观察不到低阈值内向电流。高阈值钙电流被硝苯地平(100纳摩尔)消除,并被Bay K 8644(100纳摩尔)增强。二价阳离子通过钙通道的通透顺序为钡离子大于锶离子约等于钙离子。镉离子比镍离子更有效地阻断钙电流。这些结果可能表明气管平滑肌细胞的钙电流主要由通过L型钙通道的电流组成。