Niggli E, Lederer W J
Department of Physiology, University of Bern, Switzerland.
Biophys J. 1993 Aug;65(2):882-91. doi: 10.1016/S0006-3495(93)81105-6.
Intracellular photorelease of Ca2+ from "caged calcium" (DM-nitrophen) was used to investigate the Ca(2+)-activated currents in ventricular myocytes isolated from guinea pig hearts. The patch-clamp technique was applied in the whole-cell configuration to measure membrane current and to dialyze the cytosol with a pipette solution containing the caged compound. In the presence of inhibitors for Ca2+, K+, and Na+ channels, concentration jumps of [Ca2+]i induced a rapidly activating inward Na-Ca exchange current which then decayed slowly (tau approximately 500 ms). The initial peak of the inward current and the time-course of current decay were voltage-dependent, and no reversal of the current direction was found between -100 and +100 mV. The observed shallow voltage dependence can be described in terms of the movement of an apparently fractional elementary charge (+0.44e-) across an energy barrier located symmetrically in the electrical field of the membrane. The currents were dependent on extracellular Na+ with a half-maximal activation at 73 mM and a Hill coefficient of 2.8. No change of membrane conductance was activated by the Ca2+ concentration jump when extracellular Na+ was completely replaced by Li+ or N-methyl-D-glucamine (NMG) or when the Na-Ca exchange was inhibited by extracellular Ni2+, La3+, or dichlorobenzamil (DCB). The velocity of relengthening after a twitch induced by photorelease of Ca2+ was only reduced drastically when both the sarcoplasmic reticulum and the Na-Ca exchange were inhibited suggesting that all other Ca2+ removing mechanisms have a low transport capacity under these conditions. In conclusion, we have used a novel approach to study Na-Ca exchange activity with photolysis of "caged" calcium. We found that in guinea pig heart muscle cells the Na-Ca exchange is a potent mechanism for Ca2+ extrusion, is weakly voltage-dependent (118 mV for e-fold change) and can be studied without contamination with other Ca(2+)-activated currents.
利用从“笼锁钙”(DM-硝基苯酚)进行细胞内钙释放来研究从豚鼠心脏分离出的心室肌细胞中的钙激活电流。采用膜片钳技术的全细胞模式来测量膜电流,并用含有笼锁化合物的微管溶液透析细胞质。在存在钙、钾和钠通道抑制剂的情况下,细胞内钙离子浓度的阶跃变化会诱发快速激活的内向钠钙交换电流,随后该电流缓慢衰减(时间常数约为500毫秒)。内向电流的初始峰值和电流衰减的时间进程依赖于电压,并且在-100至+100毫伏之间未发现电流方向的反转。观察到的浅电压依赖性可以用一个明显分数化的基本电荷(+0.44e-)跨越对称位于膜电场中的能垒的移动来描述。电流依赖于细胞外钠离子,在73毫摩尔时达到半数最大激活,希尔系数为2.8。当细胞外钠离子完全被锂离子或N-甲基-D-葡萄糖胺(NMG)取代时,或者当钠钙交换被细胞外镍离子、镧离子或二氯苯甲酰胺(DCB)抑制时,钙离子浓度阶跃变化不会激活膜电导的改变。由钙离子光释放诱发的一次收缩后再延长的速度仅在肌浆网和钠钙交换都被抑制时才会急剧降低,这表明在这些条件下所有其他钙离子移除机制的转运能力较低。总之,我们采用了一种新方法,通过“笼锁”钙的光解来研究钠钙交换活性。我们发现,在豚鼠心肌细胞中,钠钙交换是钙离子外排的有效机制,电压依赖性较弱(每折叠变化为118毫伏),并且可以在不被其他钙激活电流污染的情况下进行研究。