Hougaard C, Niemeyer M I, Hoffmann E K, Sepúlveda F V
August Krogh Institute, University of Copenhagen, Denmark.
Pflugers Arch. 2000 Jun;440(2):283-94. doi: 10.1007/s004240000273.
K+ and Cl- currents activated by hypoosmotic cell swelling (IK,vol and Icl,vol) or after addition of leukotriene D4 (LTD4) to cells in isotonic medium were studied in Ehrlich ascites tumour cells. IK,vol and Icl,vol were not affected by strong buffering of intracellular Ca2+ or by additional removal of extracellular Ca2+. In isotonic media, 5 nmol/l LTD4 activated large K+ but not Cl- currents. The LTD4-activated IK was, as has been shown previously for IK,vol, insensitive to charybdotoxin (ChTX) but was blocked by the antiarrhythmic drug clofilium. The current/voltage (I/V) relation for the LTD4-activated IK was, as recently demonstrated for IK,vol, well fitted by the Goldman-Hodgkin-Katz current equation between -130 mV and 30 mV in both physiological and K+-rich extracellular solutions. LTD4 had no additional effect on the magnitude of IK in Ehrlich cells already activated by the hypoosmotic stimulus. Nevertheless, the onset time for IK after hypoosmotic cell swelling was significantly less in the presence of LTD4. The similar I/V relation, pharmacological sensitivity and lack of additivity suggest that hypoosmotic swelling and addition of LTD4 activate the same K+ channels in Ehrlich cells. The influence of [Ca2+]i appears, however, to differ between IK,vol and the IK activated by LTD4 in that the latter was reduced significantly by strong buffering of [Ca2+]i. This might reflect the involvement of some additional factor in the hypoosmotic activation of K+ channels besides the stimulation mediated by LTD4.
在艾氏腹水瘤细胞中研究了低渗性细胞肿胀激活的K⁺和Cl⁻电流（IK,vol和Icl,vol），以及在等渗培养基中向细胞添加白三烯D4（LTD4）后激活的电流。IK,vol和Icl,vol不受细胞内Ca²⁺的强缓冲作用或细胞外Ca²⁺的额外去除的影响。在等渗培养基中，5 nmol/l的LTD4激活了大的K⁺电流，但未激活Cl⁻电流。如先前对IK,vol的研究所示，LTD4激活的IK对蝎毒素（ChTX）不敏感，但被抗心律失常药物氯非铵阻断。LTD4激活的IK的电流/电压（I/V）关系，如最近对IK,vol的研究所示，在生理和富含K⁺的细胞外溶液中，在-130 mV至30 mV之间，很好地符合戈德曼-霍奇金-卡茨电流方程。LTD4对已经被低渗刺激激活的艾氏细胞中的IK大小没有额外影响。然而，在存在LTD4的情况下，低渗性细胞肿胀后IK的起始时间明显缩短。相似的I/V关系、药理敏感性和缺乏叠加性表明，低渗性肿胀和添加LTD4激活了艾氏细胞中相同的K⁺通道。然而，细胞内Ca²⁺浓度（[Ca²⁺]i）的影响在IK,vol和LTD4激活的IK之间似乎有所不同，因为后者在[Ca²⁺]i的强缓冲作用下显著降低。这可能反映了除LTD4介导的刺激外，一些其他因素参与了K⁺通道的低渗性激活。
