Bronner C, Ratsimbason M, Pelen F, Landry Y
Laboratoire de Neuroimmunopharmacologie, Université Louis Pasteur, Strasbourg I, Faculté de Pharmacie, Illkirch, France.
Agents Actions. 1991 May;33(1-2):88-91. doi: 10.1007/BF01993134.
The role of the sodium pump in the plasma membrane potential changes induced by compound 48/80 and by antigenic challenge has been investigated using a fluorescent potential sensitive probe, bis-oxonol. Compound 48/80 induced a fast decrease of the fluorescence of bis-oxonol followed by a delayed decrease. The antigenic stimulation induced only a delayed decrease of fluorescence. Zinc gluconate inhibited the first decrease but did not alter the second one. The delayed decrease was inhibited by ouabain or by the absence of potassium. These results suggest that compound 48/80 induced mast cell secretion via a zinc-sensitive mechanism followed by activation of the sodium pump. The changes in the plasma membrane potential during the antigenic stimulation are due to the activation of the sodium pump but occur after the secretion process.
利用荧光电位敏感探针双缩苹果酸,研究了钠泵在由化合物48/80和抗原攻击诱导的质膜电位变化中的作用。化合物48/80引起双缩苹果酸荧光快速下降,随后是延迟下降。抗原刺激仅引起荧光延迟下降。葡萄糖酸锌抑制了首次下降,但未改变第二次下降。哇巴因或无钾状态可抑制延迟下降。这些结果表明,化合物48/80通过锌敏感机制诱导肥大细胞分泌,随后激活钠泵。抗原刺激期间质膜电位的变化是由于钠泵的激活,但发生在分泌过程之后。