Nakahari T, Fujiwara S, Shimamoto C
Department of Physiology, Osaka Medical College, Takatsuki, Japan.
J Korean Med Sci. 2000 Aug;15 Suppl(Suppl):S36-7. doi: 10.3346/jkms.2000.15.S.S36.
Effects of intracellular Na+, K+ and Cl- on Ca(2+)-regulated exocytosis activated by 10 microM acetylcholine (ACh) were studied in guinea-pig antral mucous cells which are permeabilized by nystatin treatment. Ca(2+)-regulated exocytotic events were modulated by [Na+]i, [K+]i and [Cl-]i via mediation of PTX-sensitive G proteins. Increases in [Na+]i and PTX inhibit G protein (G(Na)), which suppressed the exocytosis. Increases in [K+]i caused the exchange of G proteins (from G(Na) to G(K)) to increase, and GK evoked activation of the exocytosis and was inhibited by PTX. Increases in [Cl-]i and PTX inhibit G protein (G(Cl)), which stimulates exocytotic events. Based on these observations, the exocytosis in antral mucous cells were modulated by intracellular ions, concentration of which were increased or decreased by cell volume changes caused by Ach.
在经制霉菌素处理而通透的豚鼠胃窦黏液细胞中，研究了细胞内的Na⁺、K⁺和Cl⁻对由10微摩尔乙酰胆碱（ACh）激活的Ca²⁺调节的胞吐作用的影响。Ca²⁺调节的胞吐事件通过百日咳毒素（PTX）敏感的G蛋白介导，受到细胞内[Na⁺]、[K⁺]和[Cl⁻]的调节。细胞内[Na⁺]的增加和PTX抑制G蛋白（G(Na)），从而抑制胞吐作用。细胞内[K⁺]的增加导致G蛋白的交换（从G(Na)到G(K)）增加，并且GK引起胞吐作用的激活，并被PTX抑制。细胞内[Cl⁻]的增加和PTX抑制G蛋白（G(Cl)），而G(Cl)刺激胞吐事件。基于这些观察结果，胃窦黏液细胞中的胞吐作用受到细胞内离子的调节，这些离子的浓度因ACh引起的细胞体积变化而增加或减少。
