The membrane locus of Ca-stimulated K transport in energy depleted human red blood cells

Abstract

Energy depleted human red cells subsequently exposed to iodoacetate (IAA) develop, upon the addition of Ca, a marked increase in K permeability, while Na permeability is unaltered. The kinetic characteristics of this augmented K permeability indicate that the transport process is membrane mediated. Thus, the inward and outward rate constants for K increase as the concentration of external K is increased reaching maximum values between 2 to 5mm; further increases in external K results in a partial reduction of the rate constants. In addition, the Ca-stimulated K transport system displays counterflow of⁴²K during its influx when a large gradient of³⁹K exists (inside high, outside low). Furthermore, the Ca-induced K transport is inhibited by ouabain. The sensitivity of the Ca-induced system to ouabain parallels the action of ouabain on the Na−K pump. At least part of the increased K transport occurs through a preexisting pathway since ouabain bound to cells before exposure to Ca and IAA results in an inhibition of K outflux. Since ouabain does not alter the affinity of the cells for Ca, it is concluded that at least a portion of the increased K transport results from Ca acting to increase the turnover rate of the same system which serves as the Na−K pump in normal red cells.