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Research Article Free access | 10.1172/JCI106496
Department of Internal Medicine, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Department of Microbiology, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
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Department of Internal Medicine, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Department of Microbiology, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Find articles by Bieberdorf, F. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Department of Microbiology, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Find articles by Morawski, S. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Department of Microbiology, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
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Department of Internal Medicine, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Department of Microbiology, The University of Texas (Southwestern) Medical School at Dallas, Dallas, Texas 75235
Find articles by Fordtran, J. in: JCI | PubMed | Google Scholar
Published February 1, 1971 - More info
To assess the ion transport mechanism by which cholera causes the small bowel to secrete, ion transport rates and electrical potential difference (PD) were determined simultaneously in the normal and choleragen-treated dog ileum in vivo. The results indicate that, during cholera, HCO3 is actively secreted (i.e., against both an electrical and a concentration gradient); Cl is also actively secreted, against a modest electrochemical gradient. Electrogenic pumping of one or both of these anions is probably responsible for an observed PD change of approximately 13 mv (lumen negative). Na secretion can be accounted for entirely by passive ion movement. K secretion can be partly explained by passive diffusion secondary to the negative intraluminal PD; however, its concentration in the secreted fluid is two to three times higher than expected on the basis of passive forces, suggesting a component of active K secretion. The PD response of the choleragen-treated ileum is normal in response to glucose, but there was no PD response to saline-free mannitol perfusion. This suggests that the normal differential permeability of the ileum to anions and cations may be altered by choleragen, although other explanations of this finding are also possible.
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