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Research Article Free access | 10.1172/JCI106874

Effect of Cholera Enterotoxin on Ion Transport across Isolated Ileal Mucosa

Michael Field, David Fromm, Qais Al-Awqati, and William B. Greenough III

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Surgery, Beth Israel Hospital, Boston, Massachusetts 02215

Department of Medicine, Infectious Diseases Division, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224

Department of Medicine, Infectious Diseases Division, Baltimore City Hospitals, Baltimore, Maryland 21224

Find articles by Field, M. in: JCI | PubMed | Google Scholar

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Surgery, Beth Israel Hospital, Boston, Massachusetts 02215

Department of Medicine, Infectious Diseases Division, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224

Department of Medicine, Infectious Diseases Division, Baltimore City Hospitals, Baltimore, Maryland 21224

Find articles by Fromm, D. in: JCI | PubMed | Google Scholar

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Surgery, Beth Israel Hospital, Boston, Massachusetts 02215

Department of Medicine, Infectious Diseases Division, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224

Department of Medicine, Infectious Diseases Division, Baltimore City Hospitals, Baltimore, Maryland 21224

Find articles by Al-Awqati, Q. in: JCI | PubMed | Google Scholar

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Department of Surgery, Harvard Medical School, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Medicine, Beth Israel Hospital, Boston, Massachusetts 02215

Gastrointestinal Unit, Department of Surgery, Beth Israel Hospital, Boston, Massachusetts 02215

Department of Medicine, Infectious Diseases Division, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224

Department of Medicine, Infectious Diseases Division, Baltimore City Hospitals, Baltimore, Maryland 21224

Find articles by Greenough, W. in: JCI | PubMed | Google Scholar

Published April 1, 1972 - More info

Published in Volume 51, Issue 4 on April 1, 1972
J Clin Invest. 1972;51(4):796–804. https://doi.org/10.1172/JCI106874.
© 1972 The American Society for Clinical Investigation
Published April 1, 1972 - Version history
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Abstract

The effects of cholera enterotoxin on intestinal ion transport were examined in vitro. Addition of dialyzed filtrate of Vibrio cholerae (crude toxin) to the luminal side of isolated rabbit ileal mucosa caused a delayed and gradually progressive increase in transmural electric potential difference (PD) and shortcircuit current (SCC). A similar pattern was observed upon addition of a highly purified preparation of cholera toxin, although the changes in PD and SCC were smaller. Na and Cl fluxes across the short-circuited mucosa were determined with radioisotopes 3-4 hr after addition of crude toxin or at a comparable time in control tissues. The toxin caused a net secretory flux of Cl and reduced to zero the net absorptive flux of Na. Similar flux changes were observed when either crude or purified toxin was added in vivo and tissues were mounted in vitro 3-4 hr later. Additon of D-glucose to the luminal side of toxin-treated mucosa produced a large net absorptive flux of Na without altering the net Cl and residual ion fluxes.

Adenosine 3′,5′-cyclic phosphate (cyclic AMP) and theophylline had previously been shown to cause a rapid increase in SCC and ion flux changes similar to those induced by cholera toxin. Pretreatment of ileal mucosa with either crude or purified cholera toxin greatly reduced the SCC response to theophylline and dibutyryl cyclic AMP, which, together with the flux data, suggest that both cyclic AMP and cholera toxin stimulate active secretion by a common pathway. Inhibition of the SCC response to theophylline was observed after luminal but not after serosal addition of toxin. In vitro effects of cholera toxin correlated closely with in vivo effects: heating toxin destroyed both; two V. cholerae filtrates which were inactive in vivo proved also to be inactive in vitro; PD and volume flow measurements in isolated, in vivo ileal loops of rabbit revealed that the PD pattern after addition of toxin is similar to that seen in vitro and also correlates closely with changes in fluid movement. The results suggest that stimulation by cholera toxin of a cyclic AMP-dependent active secretory process of the intestinal epithelial cells is a major cause of fluid loss in cholera.

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