Calcium-activated chloride current in rabbit coronary artery myocytes.
Calcium-activated chloride current in rabbit coronary artery myocytes.
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兔冠状动脉肌细胞中的钙激活氯电流。
DOI：
10.1161/01.res.75.4.742
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发表时间：
1994
影响因子：
20.1
通讯作者：
Shibata,EF
中科院分区：
文献类型：
--
作者：
Lamb,FS;Volk,KA;Shibata,EF
采用全细胞膜片钳技术对酶分散的心外膜冠状动脉平滑肌细胞进行研究。从-60 mV(118 mV/L氯化铯、22 mmo1/L四乙基氯化铵、5 mmo1/L EGTA移液)起500毫秒的去极化电压脉冲可诱发内向L型钙电流(ICa)。当从移液管溶液中省略EGTA时，向外电流叠加在钙电流上，而复极化电压阶跃产生向内尾流(IT)。在-30~+50 mV范围内，这些内向电流的幅度与ICA幅度成正比。电流衰减的时间过程可用单指数方程很好地拟合。这个方程的时间常数(Tau)不随IT的大小而改变，但明显依赖于电压(较负的电位较短)。在移液管溶液中用甲烷磺酸作为氯离子的取代物，通过阴离子取代将氯离子翻转电位从-1.3 mV改变到-39.7 mV，使IT的零电流水平从0.9+/-0.56 mV移动到-33.1+/-0.85 mV。尾电流可被硝苯地平(10(-6)m ol/L)阻断，并可被等摩尔钙离子取代的Ba2+阻断，并被二氢吡啶激动剂Bay K8644(10(-6)m o l/L)增强。氯通道阻断剂DIDS(10(-4)m o l/L)和尼氟米酸(10(-5)m o l/L)也可阻断该通道。释放细胞内钙储备的咖啡因(10(-2)mol/L)在保持电位(-60 mV)引起内向电流，该电流可被DIDS抑制。咖啡因还抑制了通过使脉冲去极化而引发IT的后续尝试(IT减少88%)。
Whole-cell patch-clamp techniques were used to study enzymatically dispersed epicardial coronary artery smooth muscle cells. Depolarizing voltage pulses of 500-millisecond duration from -60 mV (118 mmol/L CsCl, 22 mmol/L tetraethylammonium chloride, and 5 mmol/L EGTA pipette solution) elicited inward L-type calcium currents (ICa). When EGTA was omitted from the pipette solution, an outward current was superimposed on the calcium current, and repolarizing voltage steps produced an inward tail current (IT). The amplitude of these inward currents was proportional to the ICa amplitude from -30 to +50 mV. The time course of decay of the current was well fit by a single exponential equation. The time constant (tau) of this equation did not change with the size of IT but was clearly voltage dependent (shorter at more negative potentials). Changing the chloride reversal potential from -1.3 to -39.7 mV by anion substitution using methanesulfonate as the chloride replacement in the pipette solution shifted the zero current level of IT from 0.9 +/- 0.56 to -33.1 +/- 0.85 mV. The tail current was blocked by nifedipine (10(-6) mol/L) and by isosmolar calcium substitution with barium in the bath solution and was enhanced by the dihydropyridine agonist Bay K 8644 (10(-6) mol/L). IT was also blocked by the chloride channel blockers DIDS (10(-4) mol/L) and niflumic acid (10(-5) mol/L). Caffeine (10(-2) mol/L), which releases intracellular calcium stores, caused an inward current at holding potentials (-60 mV), which was inhibited by DIDS. Caffeine also inhibited subsequent attempts to elicit IT by depolarizing pulses (88% reduction in IT).(ABSTRACT TRUNCATED AT 250 WORDS)