Characterization of aldosterone-induced potassium secretion in rat distal colon

Abstract

The role of apical and basolateral membranes in aldosterone-induced active potassium (K) secretion in rat distal colon was investigated by measuring mucosal-to-serosal (J(ms)) and serosal-to-mucosal (J(sm)) 42K fluxes (μeq · h-1 · cm-2) across isolated stripped mucosa under short-circuit conditions in normal and secondary-hyperaldosterone animals. In normal colons mucosal tetraethylammonium (TEA; 30 mM) or barium (Ba; 5 mM), but not cesium (Cs; 15 mM), reduced J(sm) without affecting J(ms). In aldosterone animals (a) net K secretion (-0.54 ± 0.11) was converted to net K absorption (0.63 ± 0.15) by mucosal TEA, which produced a marked reduction in J(sm) (0.82 ± 0.07) and an increase in J(ms) (0.35 ± 0.07). In contrast mucosal Ba resulted in a relatively smaller reduction in J(sm)(K) without altering J(ms)(K), whereas mucosal Cs was ineffective; (b) serosal bumetanide or the removal of serosal Na or Cl markedly inhibited J(sm)(K) and abolished net K secretion; and (c) serosal ouabain (1 mM) produced qualitatively similar effects to those of serosal bumetanide. These results demonstrate that (a) normal rat distal colon contains apical TEA- and Ba-sensitive K channels; (b) aldosterone induces TEA-sensitive and Ba-sensitive apical K channels; (c) aldosterone-induced K secretion requires both the Na,K-pump and Na-K-2Cl cotransport for K uptake across the basolateral membrane; and (d) alteration of any of these processes results in inhibition of aldosterone-induced active K secretion simultaneously with stimulation of K absorption.