在低張狀態下，多數哺乳類細胞先是體積漲大，而後恢復原來體積。此一細胞調節本身體積的功能，可能與鉀離子的運輸有關。在本實驗中，我們以血癌細胞為模型，研究其因體積變化而活化之鉀離子運輸途徑。我們發現，血癌細胞上因體積變化而活化的鉀離子運輸會受到Ouabain及Bumetanide的影響而降低，顯示此一鉀離子運輸可能與Na/sup +//K/sup +/pump及Na/sup +//K/sup +//Cl/sup -/共同運輸有關。由於此一因體積變化而活化的鉀離子運輸亦為NPPB所抑制，顯示此一因體積變化而活化的鉀離子運輸可能經由一特殊之陰離子通道(Anion channel)。而在細胞內訊息(Signaling)方面，此一因體積變化而活化的鉀離子運輸為Genistein所抑制，因此，其似乎受到tyrosine protein kinase的調節，但可能並不受到Gardos通道的影響。 Under hypoosmotic condition, most mammalian cell types undergo regulatory volume decrease (RVD) and restore their original volume. In the current study, we characterize the K/sup +/ transport in K562 leukemia cells under hypoosmolarity. The hypoosmotically-induced K/sup +/ efflux was inhibited by ouabain and bumetanide, suggesting the involvement of Na/sup +//K/sup +/ pump and Na/sup +//K/sup +//Cl/sup -/ cotransport. Anion channel blocker NPPB significantly inhibited the hypoosmotically-induced K/sup +/ efflux, suggesting the K/sup +/ efflux may also via a specific anion channel. Moreover, this hypoosmotically-induced K/sup +/ efflux was blocked by genistein, suggesting intracellular tyrosine protein kinase may regulate this hypoosmotically-induced K/sup +/ efflux. Since the hypoosmotically-induced K/sup +/ efflux was not blocked by EDTA, the involvement with Gardos channel may be unlikely.
