Potassium secretion by neonatal rat distal colon.

Electrogenic K+ secretion across the distal colon of young rats was investigated by measuring the sensitivity of the short-circuit current to Ba2+ added to the mucosal side of the tissue. Ba2+-sensitive short-circuit current (IBasc) was high during the suckling and weaning periods but very low in adult animals. Increasing the mucosal K+ concentration was accompanied by the inhibition of the serosa-to-mucosa IBasc and the induction of the mucosa-to-serosa IBasc. The IBasc was decreased by serosal omission of either Na+ or Cl- as well as by serosal addition of furosemide or ouabain. Mucosal omission of Na+ did not change IBasc. By increasing the plasma level of aldosterone (low-sodium diet) IBasc rose by 95% whereas treatment decreasing this level (high-sodium diet) reduced IBasc by 76%. Bilateral adrenalectomy lowered IBasc by 59% and treatment of adrenalectomized rats with deoxycorticosterone acetate prevented the reduction of IBasc. Tetraethylammonium and quinidine had similar effects on Isc as Ba2+. These data are consistent with the presence of a high level of K+ secretion in the distal colon of neonatal rats. This secretory pathway is electrogenic and independent of Na+ absorption. It appears to be mediated by the Na-K-ATPase as well as a furosemide-sensitive Na-Cl or Na-Cl-K cotransport on the basolateral side and by Ba2+-sensitive K+ conductive pathways on the mucosal side. The results suggest that this K+ secretion can be regulated by mineralocorticoids. The mineralocorticoids are necessary for "stimulated" K+ secretion but they are not essential for maintaining "basal" K+ secretion.