We characterized the hyperpolarization of the electrical potential profile of flounder intestinal cells that accompanies inhibition of NaCl cotransport. Several observations indicate that hyperpolarization of ψa and ψb (Δψa,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 (b) mucosal bumetanide or serosal cGMP, inhibitors of NaCl influx, elicited Δψa,b and decreased the transepithelial potential (ψt) in parallel. Regardless of initial values, ψa and ψb approached the equilibrium potential for K (EK) so that in the steady state following inhibition of NaCl entry, ψa ≅ ψb ≅ ECl ≅ EK. Bumetanide decreased cell Cl activity (aClc) toward equilibrium levels. Bumetanide and cGMP decreased the fractional apical membrane resistance (fRa), increased the slope of the relation of ψa to [K]m, and decreased cellular conductance (Gc) by ~85%, which indicates a marked increase in basolateral membrane conductance (Gb). Since the basolateral membrane normally shows a high conductance to Cl, a direct relation between apical salt entry and GClb 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 Δψa,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 Δψa,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.
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