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缓激肽可在从新生大鼠背根神经节分离出的非神经元细胞中诱发一种钙激活氯离子电流。

Bradykinin evokes a Ca2+-activated chloride current in non-neuronal cells isolated from neonatal rat dorsal root ganglia.

作者信息

England S, Heblich F, James I F, Robbins J, Docherty R J

机构信息

Novartis Institute for Medical Research, 5 Gower Place, London WC1E 6BN, UK.

出版信息

J Physiol. 2001 Feb 1;530(Pt 3):395-403. doi: 10.1111/j.1469-7793.2001.0395k.x.

Abstract

We have studied the effect of bradykinin (Bk) on fibroblast-like satellite (FLS) cells isolated from cultures of neonatal rat dorsal root ganglia (DRG). In voltage-clamped FLS cells Bk evoked an inward current response that was concentration dependent with a half-maximal concentration of 2 nM. In indo-1 AM-loaded FLS cells Bk evoked a rise in intracellular Ca2+ that was concentration dependent with a half-maximal concentration of 1 nM. The FLS cells still produced an inward current in response to Bk in the absence of extracellular Ca2+ but the response was inhibited if the intracellular concentration of EGTA was increased from 0.5 to 5 mM, which suggests that the inward current was dependent on the release and subsequent rise of intracellular Ca2+. The reversal potential of the Bk-induced inward current was consistent with the current being due to an increase in Cl- conductance and shifted in a Nernstian manner when the intracellular Cl- concentration was reduced. The inward current response to Bk was blocked by the B2 receptor antagonist HOE-140, which indicates that the response was due to activation of B2 receptors. The data suggest that Bk evokes a rise in intracellular Ca2+ and activation of a Ca2+-activated Cl- conductance in the FLS cells and raise the possibility that FLS cells contribute to the pro-inflammatory effects of Bk in DRG.

摘要

我们研究了缓激肽(Bk)对从新生大鼠背根神经节(DRG)培养物中分离出的成纤维细胞样卫星(FLS)细胞的作用。在电压钳制的FLS细胞中,Bk诱发了内向电流反应,该反应呈浓度依赖性,半数最大浓度为2 nM。在负载indo-1 AM的FLS细胞中,Bk诱发细胞内Ca2+升高,该反应呈浓度依赖性,半数最大浓度为1 nM。在无细胞外Ca2+的情况下,FLS细胞仍对Bk产生内向电流,但如果细胞内EGTA浓度从0.5 mM增加到5 mM,该反应则受到抑制,这表明内向电流依赖于细胞内Ca2+的释放及随后的升高。Bk诱导的内向电流的反转电位与该电流由Cl-电导增加所致一致,并且当细胞内Cl-浓度降低时,以能斯特方式发生偏移。对Bk的内向电流反应被B2受体拮抗剂HOE-140阻断,这表明该反应是由于B2受体的激活。这些数据表明,Bk诱发FLS细胞内Ca2+升高并激活Ca2+激活的Cl-电导,并增加了FLS细胞促成Bk在DRG中的促炎作用的可能性。

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