Intracellular [Ca2+] transients in voltage clamped cardiac Purkinje fibers.
Intracellular [Ca2+] transients in voltage clamped cardiac Purkinje fibers.
复制标题
电压钳制心脏浦肯野纤维中的细胞内 [Ca2] 瞬变。
DOI：
10.1007/bf00584312
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Isenberg,G
中科院分区：
文献类型：
--
作者：
Wier,WG;Isenberg,G
用钙激活的生物发光蛋白Aequorin观察电压钳夹犬浦肯野纤维细胞内[Ca~(2+)]的瞬变。电压钳脉冲期间的发光模式由两部分组成：L1和L2，L1是发光的快速初始增加，L2是可变构型的较慢的二次上升。1.D600(2μM)消除了L1、L2、内向电流和收缩。L1比L2更快启动，L1在100ms内启动，而L2不在100ms内启动。50ms或500ms钳位脉冲的峰值内向电流相同；50ms钳位脉冲的L1与500ms钳位脉冲的L1相同或略有降低。然而，与重复给予500ms脉冲相比，在重复给予50ms脉冲时取消了L2。当500ms脉冲与50ms脉冲交替时，50ms脉冲中的L2大于500ms脉冲中的L2。在−35~0 mV范围内，L1峰和内向电流峰几乎同时出现，具有相同的阈值电位，并且与膜电位有相似的依赖关系。在L2存在时，收缩产生的峰值张力是没有L2时的几倍，达到峰值张力的时间更长，松弛更快。由此可以得出结论：L2主要是由商店释放的钙离子造成的，而“激活剂钙”主要是从商店释放出来的。来自其他来源的Ca2+解释了L1，并激活了收缩的一小部分早期成分。L1具有与钙离子通过慢内向电流而不是通过钠/钙交换进入有关的信号的一些预期性质。
The Ca2+-activated bioluminescent protein aequorin was used to observe intracellular [Ca2+] transients in voltage clamped canine Purkinje fibers. The pattern of luminescence during a voltage clamp pulse was characterized by two components: L1, which is a rapid initial increase in luminescence and L2, which is a slower, secondary rise of variable configuration.1.L1, L2, inward current, and contraction were abolished by D 600 (2 μM).2.Paired clamp pulses. L1reprimes more rapidly than L2; L1reprimes within 100 ms, L2does not.3.Clamp pulse duration. Peak inward current was the same for 50 ms or 500 ms clamp pulses; L1was either the same or slightly reduced in 50 ms clamp pulses compared to 500 ms clamp pulses. L2, however, was abolished in repetitively given 50 ms pulses compared to repetitively given 500 ms pulses. When 500 ms pulses were alternated with 50 ms pulses, L2was greater in the 50 ms pulse than in the 500 ms pulse.4.Clamp pulse potential. In the range −35 to 0 mV, peak L1and peak inward current occurred at nearly the same time, had the same threshold potential, and had a similar dependence on membrane potential.In the presence of L2, contractions develop severalfold greater peak tension, time to peak tension is longer, and relaxation is more rapid than in the absence of L2. It is concluded that Ca2+released from stores accounts for L2and most of the ‘activator calcium’. Ca2+from another source accounts for L1and activates a small early component of the contraction. L1has some properties expected for a signal related to Ca2+entering via slow inward current, but not via Na/Ca exchange.