Relation of the Electrical Potential Profile to Coupled NaCl Absorption

Wecharacterized the hyperpolarization ofthe electrical potential profile of flounder intestinal cells that accompanies inhibition of NaCl cotransport . Several observations indicate that hyperpolarization of ~, and ~b (DY'a,b) results from inhibition of NaCl entry across the apical membrane : (a) the response was elicited by replacement of mucosal solution Cl or Na by nontransported ions, and (6) mucosal bumetanide or serosal cGMP, inhibitors of NaCl influx, elicited A~.,b and decreased the transepithelial potential (4',) in parallel . Regardless of initial values, 0, and ~b approached the equilibrium potential for K (E") so that in the steady state following inhibition of NaCl entry, ¢, a Y'b a Ec' 25 E" . Bumetanide decreased cell Cl activity (a°) toward equilibrium levels . Bumetanide and cGMP decreased the fractional apical membrane resistance (fR), increased the slope of the relation of ~a to [K],n , and decreased cellular conductance (G.) by ~85%, which indicates a marked increase in basolateral membrane conductance (Gb) . Since the basolateral membrane normally shows a high conductance to CI, a direct relation between apical salt entry and G" is suggested by these findings . As judged by the response to bumetanide or ion replacement in the presence of mucosal Ba, inhibition of Na/K/Cl co-transport alone is not sufficient to elicit AO.,b. This suggests the presence of a parallel NaCl co-transport mechanism that may be activated when Na/K/Cl co-transport is compromised . The AP.,b response to reduced apical NaCl entry would assist in maintaining the driving force for Na-coupled amino acid uptake across the apical membrane as luminal [NaCl] falls during absorption .