Modulation of high- and low-voltage-activated calcium currents in smooth muscle by calcium.

Modulation of high- and low-voltage-activated calcium currents in smooth muscle by calcium.
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钙对平滑肌中高电压和低电压激活的钙电流的调节。

DOI:
10.1152/ajpcell.1997.273.3.c883
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发表时间:
1997
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Fay,FS
Fay,FS
中科院分区:
--
文献类型:
--
作者:
McCarron,JG;McGeown,JG;WalshJr,JV;Fay,FS

文献摘要

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用全细胞电压钳和Fura 2分别测定分离的中华大蟾蜍胃肌细胞的钙电流(ICa)和胞浆钙浓度([Ca2+]c)。在去极化脉冲的条件化序列后,高压激活的ICa(测试电位+10 mV)增加,大约85 S后返回到控制值。这种增强是[Ca~(2+)]c依赖的,在大约600 nM[Ca~(2+)]c时最大增加。在条件化序列期间,在70ms测量的ICa,它提供了高压激活电流的度量,最初随着每个连续脉冲的减少而减少到序列中第一个脉冲的最小56+/-5%。此后,70ms的电流出现了相当大的恢复。用多肽(Rs20)或卡咪唑阻断钙调蛋白的活性不影响早期的抑制,但取消电流的恢复。钙调素依赖的蛋白激酶II(CK3AA)的多肽抑制剂也有类似的作用。减去在存在和不存在RS20的情况下测量的电流,发现在列车启动和电流增强开始之间存在2-S延迟。低电压激活电流(测试电位-17 mV)在条件训练后降至对照5 S的76+/-7%,这种抑制作用在35 S后恢复到92+/-4%,且不依赖于[Ca~(2+)]_c升高。
Ca2+ currents (ICa) and cytoplasmic Ca2+ concentration ([Ca2+]c) were measured in isolated gastric myocytes from Bufo marinus using whole cell voltage clamp and fura 2, respectively. After a conditioning train of depolarizing pulses, high-voltage-activated ICa (test potential of +10 mV) was increased, returning to control values after approximately 85 s. This enhancement was [Ca2+]c dependent, with a maximal increase at approximately 600 nM [Ca2+]c. During the conditioning train, ICa measured at 70 ms, which provides a measure of high-voltage-activated current, initially decreased with each successive pulse to a minimum of 56 +/- 5% of the first pulse in the train. Thereafter, the 70-ms current showed considerable recovery. Blockade of calmodulin activity with a peptide (RS20) or calmidazolium did not affect the early inhibition but did abolish current recovery. A peptide inhibitor of calmodulin-dependent protein kinase II (CK3AA) had similar effects. Substraction of currents measured in the presence and absence of RS20 revealed a 2-s delay between the start of the train and the onset of current enhancement. It was also observed that low-voltage-activated current (test potential of -17 mV) was reduced to 76 +/- 7% of control 5 s after the conditioning train; this inhibition recovered to 92 +/- 4% after 35 s and was not dependent on [Ca2+]c elevation.