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• W2059134474 abstract "Contact-mediated lysis by human natural killer cells is inhibited by a number of drugs that block the predominant K channel. In this study we have further examined the role of the K channel and the interactions between passive K and Na transport in killing. Low external Na-inhibited killing and inhibition were not due to reduce inward current through the Na channels in the target cell. A role for the Na/H antiport is suggested since amiloride inhibited killing in a dose-dependent manner that was competitive with external Na. Depolarizing the killer cell with elevated external K did not inhibit killing. On the contrary, high K0 reduced the inhibition caused by low Na0 and by the K-channel blockers quinidine, verapamil, and retinoic acid. Hyperpolarizing the killer cell with low K0 or valinomycin inhibited killing. Valinomycin, which should prevent the depolarization caused by K-channel block, did not reverse the effect of the blockers quinidine, verapamil, and 4-aminopyridine. Hence, the primary role of the K channels during killing is not maintain the negative membrane potential. On the contrary, depolarization may promote killing under conditions where killing is submaximal." @default.
• W2059134474 created "2016-06-24" @default.
• W2059134474 creator A5001764934 @default.
• W2059134474 creator A5002323313 @default.
• W2059134474 date "1989-09-01" @default.
• W2059134474 modified "2023-10-02" @default.
• W2059134474 title "Interactive effects of Na and K in killing by human natural killer cells" @default.
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• W2059134474 doi "https://doi.org/10.1016/0014-4827(89)90368-6" @default.
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