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

Active transport of amino acids and the sugar, 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 X 10(-7) M), quinidine (10(-3) M), Ba (5 X 10(-3) M) and trifluoperazine (5 X 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 too 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. 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 homoeostasis during Na-coupled transport and contributing to the driving force for sugar and amino acid absorption.