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细胞外阴离子对兔门静脉平滑肌细胞中Ca2+激活的Cl-电流衰减的调节作用

Modulation of the decay of Ca2+-activated Cl- currents in rabbit portal vein smooth muscle cells by external anions.

作者信息

Greenwood I A, Large W A

机构信息

Department of Pharmacology and Clinical Pharmacology, Cardiovascular Research Group, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.

出版信息

J Physiol. 1999 Apr 15;516 ( Pt 2)(Pt 2):365-76. doi: 10.1111/j.1469-7793.1999.0365v.x.

DOI:10.1111/j.1469-7793.1999.0365v.x
PMID:10087337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2269276/
Abstract
  1. The effects of external anions on the decay kinetics of Ca2+-activated Cl- currents (ICl(Ca)) were studied in smooth muscle cells isolated from rabbit portal vein using the perforated patch whole-cell voltage clamp technique. 2. In normal NaCl-containing external solution the decay of spontaneous Ca2+-activated Cl- currents (STICs) and Ca2+-activated Cl- 'tail' currents (Itail) was described by a single exponential with a time constant (tau) that was prolonged by external anions which are more permeable than Cl- (Br-, I- and SCN-) and accelerated by less permeant anions. However, intracellular I- did not affect the tau of STICs and Itail. 3. There was a positive correlation between the ability of an external anion to affect the decay tau of ICl(Ca) and its permeability relative to Cl-. 4. The voltage dependence of STIC and Itail decay was not affected by external or internal anions. 5. External permeating anions were not obligatory for activation of ICl(Ca) and STIC tau was not altered in Cl--free external solution. 6. Modulation of tau by mole fractions of SCN- and Cl- ions was fitted by a logistic curve, suggesting competition between SCN- and Cl- ions for a binding site. 7. In conclusion, external anions affect the decay of ICl(Ca) by a mechanism compatible with an interaction with a binding site which modulates Cl- channel kinetics.
摘要
  1. 采用穿孔膜片全细胞电压钳技术,研究了细胞外阴离子对从兔门静脉分离的平滑肌细胞中Ca2+激活的Cl-电流(ICl(Ca))衰减动力学的影响。2. 在含正常NaCl的细胞外溶液中,自发Ca2+激活的Cl-电流(STICs)和Ca2+激活的Cl-“尾”电流(Itail)的衰减可用单一指数描述,其时间常数(tau)会被比Cl-更易通透的细胞外阴离子(Br-、I-和SCN-)延长,而被通透性较低的阴离子加速。然而,细胞内I-并不影响STICs和Itail的tau。3. 细胞外阴离子影响ICl(Ca)衰减tau的能力与其相对于Cl-的通透性之间存在正相关。4. STIC和Itail衰减的电压依赖性不受细胞外或细胞内阴离子的影响。5. 细胞外通透阴离子并非ICl(Ca)激活所必需,在无Cl-的细胞外溶液中STIC的tau不变。6. SCN-和Cl-离子摩尔分数对tau的调节符合逻辑曲线,表明SCN-和Cl-离子在一个结合位点存在竞争。7. 总之,细胞外阴离子通过与一个调节Cl-通道动力学的结合位点相互作用的机制影响ICl(Ca)的衰减。

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Time course of spontaneous calcium-activated chloride currents in smooth muscle cells from the rabbit portal vein.兔门静脉平滑肌细胞中自发性钙激活氯电流的时间进程。
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