Potassium currents in canine airway smooth muscle cells.
Potassium currents in canine airway smooth muscle cells.
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犬气道平滑肌细胞中的钾电流。
DOI：
10.1152/ajplung.1990.259.6.l384
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Kotlikoff,MI
中科院分区：
文献类型：
--
作者：
Kotlikoff,MI
采用全细胞膜片钳技术研究了犬气管离体平滑肌细胞的电特性。在电流箝位模式下，电流箝位步骤不启动动作电位，但表现出明显的向外整流，当细胞加载Cs+离子和四乙基铵（TEA+）离子取代浴液中的Na+时，这种整流被消除。在电压箝位实验中，正至-45 mV的去极化激发了短暂的电压依赖的内向Ca2+电流[Am]。J. Physiol. 254 (Cell Physiol. 23): C793-C801, 1988)，然后是持续的向外电流，它没有完全失活。根据电流的反转电位和离子取代实验，确定了向外电流为K+电流。电流被进一步定义为Ca2（+）不敏感的延迟整流电流，因为它们在以下条件下保持不变：1)Ca2+电流被Mn2+或硝苯地平（10微米）完全阻断；2) Ba2+离子取代Ca2+成为向内电流载流子；3)加charybdotoxin （40 nM）或TEA+ (10 mM)。在低Ca2+缓冲容量的内溶液[0.3 mM乙二醇-双（β -氨基乙醚）-N，N,N-，N-四乙酸（EGTA）]条件下，应用甲基胆碱（100微米）或A23187（1微米）激活Ca2（+）活化钾[K(Ca)]电流。K（Ca）电流被10 mM TEA+阻断，在高细胞内Ca2+缓冲（11 mM EGTA）条件下未观察到。这些数据表明，犬气道平滑肌细胞含有电压依赖性延迟整流通道，这是膜整流和K（Ca）通道的基础，K（Ca）通道被释放细胞内Ca2+储存的药物激活。
The electrical properties of dissociated canine tracheal smooth muscle cells were examined using the whole cell patch-clamp technique. In current clamp mode, current clamp steps did not initiate action potentials but showed clear outward rectification, which was abolished when cells were loaded with Cs+ ions and when tetraethylammonium (TEA+) ions replaced Na+ in the bath solution. In voltage-clamp experiments, depolarizations positive to -45 mV evoked brief voltage-dependent inward Ca2+ currents [Am. J. Physiol. 254 (Cell Physiol. 23): C793-C801, 1988], followed by sustained outward currents, which did not completely inactivate. Outward currents were identified as K+ currents on the basis of the reversal potential of the current and by ion-substitution experiments. The currents were further defined as Ca2(+)-insensitive delayed rectifier currents, since they were unaltered under conditions in which 1) the Ca2+ current was completely blocked by Mn2+ or nifedipine (10 microM); 2) Ba2+ ions were substituted for Ca2+ as the inward current charge carrier; or 3) charybdotoxin (40 nM) or TEA+ (up to 10 mM) were added to the bath. A Ca2(+)-activated potassium [K(Ca)] current was activated by application of methacholine (100 microM), or A23187 (1 microM), under conditions of low Ca2+ buffering capacity in the internal solution [0.3 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N-,N--tetraacetic acid (EGTA)]. The K(Ca) current was blocked by 10 mM TEA+ and was not observed under conditions of high intracellular Ca2+ buffering (11 mM EGTA). These data indicate that canine airway smooth muscle cells contain voltage-dependent delayed rectifier channels that underlie membrane rectification and K(Ca) channels that are activated by agents which release intracellular Ca2+ stores.