Effects of Na-coupled alanine transport on intracellular K activities and the K conductance of the basolateral membranes ofNecturus small intestine

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Abstract
Intracellular electrical potentials and K activity, (K) c , were determined simultaneously inNecturus small intestine before and after the addition of alanine to the mucosal solution. As noted previously (Gunter-Smith, Grasset & Schultz, 1982), the addition of alanine to the mucosal solution resulted in a prompt depolarization of the electrical potential difference across the apical membrane (ψmc) and a decrease in the slope resistance of that barrier (r m). This initial response was followed by a slower repolarization of ψmc associated with a decrease in the slope resistance of the basolateral membrane (r s) so that when the steady state was achieved (r m/r s) did not differ significantly from control values in the absence of alanine. In the absence of alanine, ψmc averaged −32 mV and(K) c averaged 67mm. When a steady state was achieved in the presence of alanine these values averaged −24 mV and 50mm, respectively. The steady-stateelectrochemical potential differences for K across the basolateral membrane in the absence and presence of alamine did not differ significantly. Inasmuch as the rate of transcellular active Na transport or “pump activity” was increased two-to threefold in the presence of alanine, it follows that,if active Na extrusion across the basolateral membrane is coupled to active K uptake across that barrier with a fixed stoichiometry then, the decrease inr s must be due to an increase in the conductance of the basolateral membrane to K that parallels the increase in “pump activity”. This “homocellular” regulatory mechanism serves to (i) prevent an increase in (K) c due to an increase in pump activity; and (ii) repolarize ψmc and thus restore the electrical driving force for the rheogenic Na-coupled entry processes.