Effects of luminal salt concentration on electrical pathways in Necturus antrum

By use of microelectrode techniques the electrical resistances of the cell membranes and paracellular pathways of surface epithelium in Necturus antrum were determined under control conditions (Ringer solutions containing 106.6 mM Na⁺, 91.4 mM Cl^-) and during exposure to mucosal solutions containing high Na⁺ and Cl^- concentrations. Resistances were determined by briefly exposing tissues to mucosal solutions containing 10^-4 M amiloride, a reversible inhibitor of Na⁺ conductances. Under control conditions in eight tissues, measurements obtained by exposure to amiloride were not significantly different from those obtained by an independent method, intraepithelial cable analysis, thus indicating the validity of the measurements obtained by the amiloride method. In 10 tissues, high luminal NaCl concentrations (Ringer salts + 125 mM NaCl) increased the apical cell membrane resistance from 5,778 ± 267 to 7,714 ± 422 Ω·cm² (P < 0.01) and the basolateral membrane resistance from 2,973 ± 186 to 3,869 ± 335 Ω·cm² (P < 0.01). The resistance of the paracellular pathway decreased from 625 ± 13 to 505 ± 13 Ω·cm² (P < 0.001). Similar alterations in these resistances were observed when Na⁺ or Cl^- were increased individually, when added as salts of isethionate^- and N-methyl-D-glucamine⁺, respectively. These effects were not attributable to increases in luminal osmolarity, since mucosal solutions made equally hyperosmotic with 250 mM sucrose elicited increases in paracellular pathway resistance and decreases in resistances of the cell membranes. The paracellular pathway thus does not limit passive permeation of Na⁺ or Cl^- through this epithelium, whereas permeation of these ions is increasingly limited at higher luminal salt concentrations. The changes in cell membrane resistance under these conditions may reflect homeostatic mechanisms that preserve cell volume and ion composition, possibly in response to alterations in composition and dimensions of the paracellular pathway.