Quinine inhibits multiple Na⁺ and K⁺ transport mechanisms in Ehrlich ascites tumor cells

The interaction of quinine with K⁺ and Na⁺ transport mechanisms has been investigated in Ehrlich ascites tumor cells. Quinine affects both Ca²⁺-dependent K⁺ channel and total K⁺ influx. Activation of Ca⁺-dependent K⁺ channels by propranolol is abolished by quinine (1 mM). In addition, quinine inhibits the ouabain-sensitive component of K⁺ influx with an apparent K_i of 0.32 ± 0.02 mM and the furosemide-sensitive component with a K_i of 0.24 ± 0.01 mM. Furthermore, a significant fraction (52%) of Na⁺ influx is inhibited by quinine. The same component is sensitive to amiloride, suggesting that it represents Na⁺/H⁺ antiport. Concomitant with the inhibition of K⁺ and Na⁺ transport, quinine stimulates ATP hydrolysis by 57%. The results suggest that quinine exerts broad, nonspecific effects on cellular mechanisms which serve to regulate cation transport in Ehrlich cells.