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 mMl), 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.
Footnotes
- Received March 15, 1972.
- Accepted July 14, 1972.
- © 1972 by The Williams & Wilkins Co.
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