Foskett J K, Wong M M, Sue-A-Quan G, Robertson M A
Division of Cell Biology, Hospital for Sick Children, Toronto, Ontario, Canada.
J Exp Zool. 1994 Feb 1;268(2):104-10. doi: 10.1002/jez.1402680206.
Stimulation of salivary secretion is associated with a rise of [Ca2+]i in acinar cells. We examined the osmotic and ionic consequences of activation of Ca(2+)-dependent K+ and Cl- channels, by simultaneous optical determinations of cell volume and [Ca2+]i, [Cl-]i or [Na+]i during muscarinic stimulation of single salivary acinar cells, using a differential interference contrast (DIC)-fluorescence microscope. Carbachol caused a rapid rise of [Ca2+]i, as well as a substantial cell shrinkage. Despite variability in the level and kinetics of the subsequent sustained phase of the [Ca2+]i response, cell volume was correlated with [Ca2+]i in all cases. Elevated [Ca2+]i was both necessary and sufficient to cause these changes in cell volume. The proposition that changes in cell volume reflected changes in cell solute content was confirmed by simultaneously measuring [Cl-]i and cell volume. Simultaneous determinations of cell volume and [Na+]i indicated that the initial cell shrinkage was due entirely to K+ and Cl- efflux. Subsequent to the initial shrinkage, [Na+]i rose to high levels, primarily due to activation of Na+/H+ exchange. Thus, modulation of ion transport activities under isosmotic conditions results in substantial changes in cell solute content and cell volume. Subsequent to the early Ca(2+)-induced changes in these parameters, other transporters become active, but it is unclear what signals their activation. Cell swelling by osmotic dilution of the bath resulted in compensatory cell shrinkage (RVD) which was sensitive to K+ and Cl- gradients. Nevertheless, a rise of [Ca2+]i was not necessary for RVD. Osmotic shrinkage and/or cell acidification were insufficient to activate Na+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)
唾液分泌的刺激与腺泡细胞内[Ca2+]i的升高有关。我们通过在使用微分干涉对比(DIC)-荧光显微镜对单个唾液腺泡细胞进行毒蕈碱刺激期间,同时光学测定细胞体积和[Ca2+]i、[Cl-]i或[Na+]i,研究了Ca(2+)依赖性K+和Cl-通道激活的渗透和离子后果。卡巴胆碱导致[Ca2+]i迅速升高,以及细胞显著收缩。尽管[Ca2+]i反应随后持续阶段的水平和动力学存在差异,但在所有情况下细胞体积都与[Ca2+]i相关。升高的[Ca2+]i对于引起这些细胞体积变化既是必要的也是充分的。通过同时测量[Cl-]i和细胞体积,证实了细胞体积变化反映细胞溶质含量变化这一观点。细胞体积和[Na+]i的同时测定表明,最初的细胞收缩完全是由于K+和Cl-外流。在最初收缩之后,[Na+]i升至高水平,主要是由于Na+/H+交换的激活。因此,在等渗条件下离子转运活动的调节导致细胞溶质含量和细胞体积的显著变化。在这些参数早期由Ca(2+)引起变化之后,其他转运体变得活跃,但不清楚是什么信号激活它们。通过对浴液进行渗透稀释使细胞肿胀导致了对K+和Cl-梯度敏感的代偿性细胞收缩(RVD)。然而,RVD并不需要[Ca2+]i升高。渗透收缩和/或细胞酸化不足以激活Na+内流。(摘要截断于250字)