Park K P, Beck J S, Douglas I J, Brown P D
Cell Physiology and Renal Research Groups, School of Biological Sciences, University of Manchester, United Kingdom.
J Membr Biol. 1994 Aug;141(2):193-201. doi: 10.1007/BF00238253.
The volumes of acinar cells isolated from rat lacrimal gland were measured on computer by video-imaging. Cells were found to swell on exposure to hypotonic solutions; they subsequently exhibited a regulatory volume decrease (RVD). RVD was inhibited in the absence of extracellular Ca2+, and by the K+ channel blocker tetraethylammonium chloride (2 mM TEA+). The possible involvement of K+ channels in RVD was further investigated in cell-attached patches. Exposing the cells to a hypotonic solution activated channels with a conductance of 141 +/- 6 pS (n = 11). These channels were partially blocked by 0.5 mM TEA+, and channel activation was not observed in the absence of extracellular Ca2+. Experiments in the inside-out patch configuration demonstrated that the channels activated by hypotonic stress were "maxi" Ca(2+)-activated K+ channels. It is concluded that the opening of these channels plays an important role in RVD, by facilitating K+ loss from the cell.
通过视频成像在计算机上测量从大鼠泪腺分离的腺泡细胞的体积。发现细胞在暴露于低渗溶液时会肿胀;随后它们表现出调节性体积减小(RVD)。在没有细胞外Ca2+的情况下以及通过K+通道阻滞剂四乙铵氯化物(2 mM TEA+),RVD受到抑制。在细胞贴附片膜中进一步研究了K+通道在RVD中的可能作用。将细胞暴露于低渗溶液会激活电导为141±6 pS的通道(n = 11)。这些通道被0.5 mM TEA+部分阻断,并且在没有细胞外Ca2+的情况下未观察到通道激活。内面向外膜片钳配置的实验表明,由低渗应激激活的通道是“大电导”Ca(2+)激活的K+通道。得出的结论是,这些通道的开放通过促进K+从细胞中流失,在RVD中起重要作用。