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Ca2+内流对单个肠平滑肌细胞中卡巴胆碱诱导的[Ca2+]i振荡的调节作用。

Modulation of carbachol-induced [Ca2+]i oscillations by Ca2+ influx in single intestinal smooth muscle cells.

作者信息

Komori S, Iwata M, Unno T, Ohashi H

机构信息

Department of Veterinary Science, Faculty of Agriculture, Gifu University, Japan.

出版信息

Br J Pharmacol. 1996 Sep;119(2):245-52. doi: 10.1111/j.1476-5381.1996.tb15978.x.

Abstract
  1. Oscillations of cytosolic Ca2+ concentration ([Ca2+]i) evoked by carbachol (CCh; 2 microM), a muscarinic agonist, were detected as oscillatory changes of muscarinic receptor-coupled cationic current (Icat) in guinea-pig ileal smooth muscle cells by the whole cell patch-clamp technique. 2. Reduction of extracellular Ca2+ from 2 mM to 0.2 or 0.05 mM, during CCh-induced Icat oscillations, caused them to disappear or to decrease markedly in frequency. A return to 2 mM Ca2+ concentration restored the initial Icat oscillations. 3. Application of nifedipine (1-3 microM) or D600 (2-5 microM) to block the voltage-gated Ca2+ channel (VGCC) decreased the frequency of the ongoing Icat oscillations in the cells held at -20 mV, but it was without effect in cells held at -60 mV. 4. Displacement of the holding potential of -20 mV to -60 mV to deactivate VGCC produced a decrease, an increase or no noticeable change in the frequency of the Icat oscillations in different cells. Displacement to 20 mV to inactivate VGCC invariably produced a decrease in the frequency. In nifedipine-treated cells, the Icat oscillations varied in frequency voltage-dependently in a reverse and linear way within the range -80 to 40 mV. 5. Application of thapsigargin (1 or 2 microM), an inhibitor of Ca(2+)-ATPase in the membrane of internal Ca2+ stores, caused CCh-induced Icat oscillations to disappear with a progressing phase during which their amplitude, but not frequency, declined. 6. The results suggest that membrane Ca2+ entry has a crucial role to play in regulation of the frequency of CCh-induced [Ca2+]i oscillations in addition to persistence of their generation, and that the effect is brought about by a potential mechanism independent of Ca2+ store replenishment. They also provide evidence that two types of Ca2+ permeant channels, VGCC and an as yet unidentified channel, are involved in the Ca2+ entry responsible for modulation of [Ca2+]i oscillations.
摘要
  1. 通过全细胞膜片钳技术,在豚鼠回肠平滑肌细胞中,检测到毒蕈碱激动剂卡巴胆碱(CCh;2微摩尔)诱发的胞质Ca2+浓度([Ca2+]i)振荡,表现为毒蕈碱受体偶联阳离子电流(Icat)的振荡变化。2. 在CCh诱导的Icat振荡期间,将细胞外Ca2+浓度从2毫摩尔降至0.2或0.05毫摩尔,导致振荡消失或频率显著降低。恢复到2毫摩尔Ca2+浓度可使初始Icat振荡恢复。3. 应用硝苯地平(1 - 3微摩尔)或D600(2 - 5微摩尔)阻断电压门控Ca2+通道(VGCC),可降低保持在-20毫伏的细胞中正在进行的Icat振荡频率,但对保持在-60毫伏的细胞无影响。4. 将保持电位从-20毫伏变为-60毫伏以使VGCC失活,在不同细胞中Icat振荡频率可降低、增加或无明显变化。变为20毫伏以使VGCC失活总是导致频率降低。在硝苯地平处理的细胞中,在-80至40毫伏范围内,Icat振荡频率呈反向线性电压依赖性变化。5. 应用毒胡萝卜素(1或2微摩尔),一种内质网Ca2+储存膜上Ca(2+)-ATP酶的抑制剂,导致CCh诱导的Icat振荡消失,在此过程中其振幅下降但频率不变。6. 结果表明,膜Ca2+内流除了在CCh诱导的[Ca2+]i振荡的产生持续性方面起关键作用外,在调节其频率方面也起关键作用,且这种作用是由一种独立于Ca2+储存补充的电位机制实现的。它们还提供证据表明,两种类型的Ca2+通透通道,VGCC和一种尚未鉴定的通道,参与了负责调节[Ca2+]i振荡的Ca2+内流。

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