The modulation by glucose transport of the electrical responses to hypertonic solutions of the goldfish intestinal epithelium.

Goldfish intestinal epithelium responds to mucosal hypertonicity with a negative biphasic transepithelial potential change and a relatively slow rise in transepithelial resistance, similar to that described for rabbit gallbladder (Wright et al. 1972; Smulders et al. 1972). In addition, the increase in resistance in goldfish intestine can be modulated by the presence or absence of glucose. E.g. during mucosal hypertonicity of 87 mosmoles/l the addition of 27.8 mmoles/l glucose to the serosal side further increased the resistance by 2.8 +/- 0.2 omega cm2, while mucosal addition reduced it by 11.2 +/- 2.6 omega cm2. Ouabain poisoning inverted this last response into a slowly and continuously rising resistance. The resistance response to mucosal glucose can be fully abolished by mucosal addition of phlorizin. The resistance change due to bilateral glucose addition is the sum of the separate mucosal and serosal responses. The effect of fructose at the serosal side resembles that of glucose added serosally; the mucosal effect of glucose could not be mimicked by fructose, but the decrease induced was of the same magnitude as the serosal effect of glucose, but of opposite sign. The effects of serosal addition of glucose and fructose and mucosal addition of fructose can be explained by different reflection coefficients of the cell membranes for glucose, fructose and mannitol. The mucosal effect of glucose is explained by a glucose-dependent influx of sodium at the mucosal side, stimulating a ouabain-sensitive pump at the baso-lateral aspects of the cell.