Abstract
Active K+ secretion in guinea pig distal colon was studied in vitro in Ussing chambers. Changes in short-circuit current (Isc), transepithelial conductance (Gt), and the unidirectional flux of 42K from serosa to mucosa (JKsm) were determined under a variety of physiological and pharmacological conditions. Mucosal tetraethylammonium (TEA) (10 or 30mM) increased Isc, while it decreased Gt and JKsm. Seroal bumetanide (10-4M) also caused an increase in Isc and decreases in Gt and JKsm. The effects produced by TEA were abolished in the presence of bumetanide. The increase in Isc caused by bumetanide was greatly reduced by mucosal high-K+ conditions. Isoproterenol (10-6M), a β-adrenergic agonist, elicited a decrease in Isc and an increase in Gt. Responses to isoproterenol (10-6M) were reduced or abolished by mucosal TEA, serosal bumetanide, serosal ouabain (10-4M), and serosal Na+- or Cl--free conditions. Mucosal high K+ also reduced the isoproterenol-induced decrease in Isc. These results suggest that K+ secretion is electrogenic and dependent on the bumetanide-sensitive cotransport in the basolateral membrane. K+ exit across the apical membrane might be conductive and sensitive to TEA. In addition, β-adrenergic agonists might stimulate K+ secretion.
