BACKGROUND & AIMS: Net sodium absorption from oral rehydration solution is increased by both glucose-sodium cotransport and solvent drag. The aim of this study was to measure the relative importance of glucose-sodium cotransport and solvent drag in the stimulation of net sodium absorption by oral rehydration solution. METHODS: Total intestinal perfusion was used in normal subjects with and without intrajejunal cholera toxin using three test solutions containing 100 mmol/L sodium and either 100 mmol/L mannitol (control), 100 mmol/L glucose, or no additional solute (hypotonic solution). The increase in sodium absorption greater than control with hypotonic solution represented sodium absorption stimulated by solvent drag; the further increase in sodium absorption induced by glucose, greater than that noted with the hypotonic solution, represented sodium absorption stimulated by cotransport. RESULTS: Without cholera toxin, solvent drag and cotransport promoted sodium absorption at rates of 62 and 33 mmol/h, respectively. With cholera toxin, solvent drag and cotransport promoted sodium absorption at rates of 44 and 71 mmol/h, respectively. CONCLUSIONS: Net sodium absorption caused by cotransport increased more than twofold after exposure of the intestine to cholera toxin (P < 0.003). This could be mediated by increased cotransport, a change in the stoichiometry of cotransport, or an increase in chloride permeability.
BACKGROUND & AIMS: Net sodium absorption from oral rehydration solution is increased by both glucose-sodium cotransport and solvent drag. The aim of this study was to measure the relative importance of glucose-sodium cotransport and solvent drag in the stimulation of net sodium absorption by oral rehydration solution. METHODS: Total intestinal perfusion was used in normal subjects with and without intrajejunal cholera toxin using three test solutions containing 100 mmol/L sodium and either 100 mmol/L mannitol (control), 100 mmol/L glucose, or no additional solute (hypotonic solution). The increase in sodium absorption greater than control with hypotonic solution represented sodium absorption stimulated by solvent drag; the further increase in sodium absorption induced by glucose, greater than that noted with the hypotonic solution, represented sodium absorption stimulated by cotransport. RESULTS: Without cholera toxin, solvent drag and cotransport promoted sodium absorption at rates of 62 and 33 mmol/h, respectively. With cholera toxin, solvent drag and cotransport promoted sodium absorption at rates of 44 and 71 mmol/h, respectively. CONCLUSIONS: Net sodium absorption caused by cotransport increased more than twofold after exposure of the intestine to cholera toxin (P < 0.003). This could be mediated by increased cotransport, a change in the stoichiometry of cotransport, or an increase in chloride permeability.
Authors: C Högenauer; C A Santa Ana; J L Porter; M Millard; A Gelfand; R L Rosenblatt; C B Prestidge; J S Fordtran Journal: Am J Hum Genet Date: 2000-10-30 Impact factor: 11.025