細胞如何在變動的環境中調節其體積，是細胞的重要功能之一。本計劃探討與調節細胞體積有密切關係的因體積而活化之鉀離子運輸 (volume-activated K+ transport) 系統。本計劃結果顯示將血癌細胞置於低張溶液中會引起大量因因體積而活化之鉀離子運輸。這些因體積而活化之鉀運輸活性並不會被 EGTA溶液或鈣離子活化之鉀離子通道 (Ca2+-activated K+ channel)抑制劑所抑制。此一因體積而活化之鉀運輸活性可以為 [(dihydroindenyl)oxy]alkanoic acid 及 bumetanide 所抑制，顯示此一因體積而活化之鉀運輸可能牽涉鉀氯共同運輸 (KCl cotransporter)及鈉鉀氯共同運輸 (Na+/K+/Cl- cotransporter)。而將血癌細胞置於低張溶液中會引起細胞的調節性細胞體積減少的反應也為 [(dihydroindenyl)oxy]alkanoic acid 及 bumetanide 所抑制。綜合以上的結果，我們可以獲知鉀氯共同運輸及鈉鉀氯共同運輸對於血癌細胞的體積調節機轉及因體積而活化之鉀離子運輸有重要的貢獻。
The characterization of volume-activated K+ flux in the leukemia cells was investigated in the current study. Exposed cells to hypoosmotic solutions significantly increased a K+ flux. This volume-activated K+ flux was not affected by incubating with EGTA solution or by treating with Ca2+-activated K+ channel blockers. This volume-activated K+ flux was demonstrated to be mainly Cl-dependent. The Cl-dependent K+ flux pathway was activated by hypoosmotic stimulation and was sensitive to both [(dihydroindenyl)oxy]alkanoic acid and bumetanide, suggesting that this K+ flux was maybe mediated by the KCl cotransporter as well as the Na/K/Cl cotransporter. The regulatory volume decrease response of cells under hypoosmolarity was also significantly inhibited by [(dihydroindenyl)oxy]alkanoic acid and bumetanide. These results suggest that the KCl cotransporter and the Na/K/Cl cotransporter play significant roles on volume regulation in leukemia cells.
