Abstract

9-Aminoacridine (9AA), a planar molecule of about 36 sq. Å, asymmetrically blocked resting ⁴²K exchange in frog sartorius muscles bathed in chloride-free or chloride-containing solutions. ⁴²K efflux was depressed more by 9AA than was uptake. The blockade by 9AA (0.01-1.0 mM) occurred when the muscles were in Na-free solutions and was unaffected by strophanthidin (10^-5M). 9AA had no effect on resting ²²Na exchange, ²²Na extrusion or the Na content of the muscles. Elevation of [K⁺]_o from 2.5 to 50 mM in chloride-free solutions or at constant [K⁺]_o x [Cl^-]_o caused an increase in the uptake and efflux of ⁴²K but the blockade of ⁴²K exchange caused by 9AA was not overcome by elevating [K⁺]_o. Like 9AA, barium (Ba⁺⁺; 0.01-1.0 mM) selectively blocked resting ⁴²K exchange. Unlike 9AA, Ba⁺⁺ reduced ⁴²K uptake and efflux symmetrically and the blockade was overcome by elevating [K⁺]_o. The uptake and efflux of ⁸⁶Rb were lower than that of ⁴²K and were more resistant to blockade By 9AA and Ba⁺⁺. Neither 9AA nor Ba⁺⁺ a tered the resting membrane potential in chloride-containing solutions ([K⁺]_o ≥ 2.5 mM^l), but both molecules caused a marked depolarization in chloride-free solutions. The depolarization produced by both 9AA and Ba⁺⁺ was associated with a reduced permeability of the membrane to K⁺. The reduction of the permeability of the membrane to K⁺ caused by Ba⁺⁺ was suggestive of a competitive interaction between Ba⁺⁺ and K⁺ for membrane sites whereas the reduction produced by 9AA was suggestive of an uncompetitive interaction.