Potassium movements associated with amino acid and sugar transport in enterocytes isolated from rabbit jejunum.

Abstract

Active transport of amino acids and the sugars, .alpha.-methyl-D-glucoside (.alpha.-MG) caused an increase in the rate of K efflux from isolated rabbit enterocytes. These effects were inhibited by apamin (5 .times. 10-7 M), quinidine (10-3 M), Ba (5 .times. 10-3 M) and trifluoperazine (5 .times. 10-5 M) but not by the loop diuretic furosemide (10-4 M). None of these drugs affected the basal rate of K efflux. The stimulatory effects of amino acids or .alpha.-MG on K efflux are to great to be explained in terms of an increase in the electrical driving force across the plasma membrane of these cells and a change in membrane permeability is envisaged. An apparent Ca-dependent K permeability in isolated enterocytes can be demonstrated using the Ca ionophore A23187 (calcimycin). The effect of the ionophore on K efflux is abolished by apamin or Ba. It is proposed that Ca-dependent K channels mediate the sugar and amino acid induced increases of K efflux. Under control conditions there is a decrease in intracellular K concentration during accumulation of alanine or .alpha.-MG. Ba by itself does not alter K concentration but it did produce a marked increase when used in conjunction with alanine or .alpha.-MG. The accumulation of .alpha.-MG was inhibited in the presence of Ba. This is consistent with an interference with the driving force for sugar accumulation. It is suggested that the increase in K permeability described has a role in both maintaining ion homeostasis during the Na-coupled transport and contributing to the driving force for sugar and amino acid absorption.