Hunter D R, Haworth R A, Goknur A B, Hegge J O, Berkoff H A
J Mol Cell Cardiol. 1986 Nov;18(11):1125-32. doi: 10.1016/s0022-2828(86)80038-4.
Anthopleurin-A stimulated the initial rate of 201thallium uptake by isolated adult rat heart cells by a factor of 3.41 +/- 0.56, and induced a unique pattern of spontaneous beating activity. Ouabain inhibited the basal uptake rate by 58 +/- 11% and all the anthopleurin-A stimulated rate. The Km for thallium uptake was 0.95 +/- 0.26 mM, and was not changed by anthopleurin-A. Accumulated thallium was quickly released from cells by EDTA addition. Such release was inhibited 87 +/- 10% by verapamil. Thallium reuptake was initiated by restoration of magnesium to the medium. Reuptake was mostly inhibited by ouabain, but the residual ouabain-insensitive uptake remained. The ouabain-insensitive uptake was inhibited by ATP depletion. Anthopleurin-A stimulated the rate of 22Na entry into cells by a factor of 3.17 +/- 1.65, and EDTA stimulated the rate of entry by a factor of 29.5 +/- 13.0. The EDTA-induced 22Na entry was inhibited 86 +/- 11% by verapamil. From this we draw three conclusions: The major pathway for thallium uptake is the Na-K pump. The rate of uptake by this route, like the rate of K+ uptake, is governed by the rate of cellular sodium influx; A residual ouabain-insensitive uptake route also exists which appears to require ATP but not a monovalent ion gradient; Removal of Mg and Ca induces a verapamil-sensitive monovalent channel activity which is both massive and reversible.
海葵毒素A使成年大鼠离体心脏细胞对铊的初始摄取速率提高了3.41±0.56倍，并诱导出独特的自发搏动活动模式。哇巴因使基础摄取速率降低了58±11%，并完全抑制了海葵毒素A刺激的摄取速率。铊摄取的米氏常数为0.95±0.26 mM，且不受海葵毒素A的影响。加入乙二胺四乙酸（EDTA）后，细胞内积累的铊迅速释放。维拉帕米可抑制这种释放，抑制率为87±10%。通过向培养基中恢复镁离子来启动铊的再摄取。再摄取大多被哇巴因抑制，但仍存在残余的对哇巴因不敏感的摄取。对哇巴因不敏感的摄取被ATP耗竭所抑制。海葵毒素A使22Na进入细胞的速率提高了3.17±1.65倍，EDTA使进入速率提高了29.5±13.0倍。维拉帕米可抑制EDTA诱导的22Na进入，抑制率为86±11%。由此我们得出三个结论：铊摄取的主要途径是钠钾泵。该途径的摄取速率，如同钾离子摄取速率一样，受细胞钠内流速率的控制；还存在一条残余的对哇巴因不敏感的摄取途径，该途径似乎需要ATP，但不需要单价离子梯度；去除镁离子和钙离子会诱导出一种对维拉帕米敏感的单价通道活性，这种活性既大量存在又可逆。
