Modification of Intestinal Secretion in Experimental Cholera

Ht, Norris; Pf, Curran; Sg, Schultz

doi:10.1093/infdis/119.2.117

Cited by 40 publications

(9 citation statements)

References 24 publications

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“…Thus, sodium exit across the serosal surface of the intestinal epithelial cell may require Na-K-ATPase regardless of the mode of sodium entry across the luminal membrane (1). Our finding that the Na-K-ATPase enzyme system was unaffected by and acted independently of choleragen-induced intestinal secretion, then, may be relevant to several previous studies which showed that intraluminal glucose can overcome ongoing cholera enterotoxin-induced intestinal secretion both in vivo (23)(24)(25) and in vitro (19). These studies have been interpreted as indicating that glucosedependent sodium absorption is intact during cholera enterotoxin-induced secretion.…”

Section: Resultssupporting

confidence: 72%

Prevention and reversal of cholera enterotoxin-induced intestinal secretion by methylprednisolone induction of Na+-K+-ATPase.

Charney

Donowitz

1976

J. Clin. Invest.

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Section: Resultssupporting

confidence: 72%

Prevention and reversal of cholera enterotoxin-induced intestinal secretion by methylprednisolone induction of Na+-K+-ATPase.

Charney

Donowitz

1976

J. Clin. Invest.

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“…Since the residual ion flux did not increase significantly after cholera toxin (see Table I), the in vitro results suggest that cholera toxin does not have a major effect on the rate of active HCO3 secretion. In the intact animals, on the other hand, most of the anion secreted into the ileum in response to cholera toxin is HCO3 and not Cl (3,26,28). Although HCO3 is also secreted by the normal ileum (29)(30)(31)(32), its rate of secretion is greatly increased by cholera toxin (1,3,26).…”

Section: Resultsmentioning

confidence: 99%

Effect of Cholera Enterotoxin on Ion Transport across Isolated Ileal Mucosa

Field¹,

Fromm²,

Al‐Awqati³

et al. 1972

J. Clin. Invest.

312

137

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A B S T R A C T 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 C1 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. Addition of D-glucose to the

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“…The inhibition of both processes by the serosal application of the stilbene SITS (White, 1980;Imon & White, 1981) Cl--HCO3-exchange mechanism like that in erythrocytes (Cabantchik & Rothstein, 1972). If the anion fluxes are linked in this way then inhibition of HCO3--dependent Cl-absorption by theophylline ( Leitch & Burrows, 1968;Norris et al 1969;Moore et al 1971) which is reduced by administration of acetazolamide (Leitch, Iwert & Burrows, 1966;Norris et al 1969). This was not demonstrable in in vitro mammalian small intestine (Field, 1974).…”

Section: Discussionmentioning

confidence: 99%

The effect of theophylline on intestinal bicarbonate transport measured by pH stat in Amphiuma.

Imon¹,

White²

1981

The Journal of Physiology

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SUMMARY1. The influence of theophylline on the mucosa to serosa and serosa to mucosa fluxes of HCO3-were measured by the pH stat technique in isolated segments of proximal small intestine from Amphiuma maintained under short-circuited conditions. The mucosal or serosal fluid was exposed to media containing 25 mM-HCO3-(pH 7 4) while the pH of unbuffered media in the opposite compartment was maintained by addition of acid.2. Theophylline significantly increased the secretary flux ofHCO3-and significantly reduced the absorptive flux when measured in Cl--free (SO42-) media.3. In normal media theophylline did not alter the secretary flux but significantly lowered the absorptive flux of HCO3-.4. Acetazolamide (041 mM) inhibited the theophylline-stimulated secretary flux of HCO3-and reduced the effect of theophylline on the absorptive flux.5. In normal intestine there was an inequality between the secretary or absorptive HCO3-flux and the short-circuit current (IS) consistent with the presence of Clabsorption. After addition of theophylline the ISc was more nearly equal to the net secretary or absorptive HCO3-flux.6. Exogenous cyclic AMP had effects identical with theophylline. 7. The results provide strong evidence that elevation of cyclic AMP stimulates net HCO3-secretion in urodele small intestine and provide indirect evidence that Clabsorption is simultaneously reduced.

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Modification of Intestinal Secretion in Experimental Cholera

Cited by 40 publications

References 24 publications

Prevention and reversal of cholera enterotoxin-induced intestinal secretion by methylprednisolone induction of Na+-K+-ATPase.

Prevention and reversal of cholera enterotoxin-induced intestinal secretion by methylprednisolone induction of Na+-K+-ATPase.

Effect of Cholera Enterotoxin on Ion Transport across Isolated Ileal Mucosa

The effect of theophylline on intestinal bicarbonate transport measured by pH stat in Amphiuma.

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