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

Charney, Alan N.; Donowitz, Mark

doi:10.1172/jci108429

Cited by 71 publications

(18 citation statements)

References 22 publications

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“…This increase in sensitivity to cholera toxin by neonatal rats could not be explained by receptor binding or density but appeared to be associated with a three-to fivefold increase in Na+,K+-ATPase enzyme activity between newborn and adult and cortisone-treated neonatal groups ( 19). Other studies have shown that rat ileum pretreated with glucocorticoids absorbed more fluid than untreated controls (34) and that rabbits deficient in glucocorticoids exhibited depressed Na+ absorption and increased Cl-secretion (35). This present study confirmed our earlier findings.…”

Section: Discussionmentioning

confidence: 76%

Expression and developmental regulation of Na+,K+ adenosine triphosphatase in the rat small intestine.

Zemelman¹,

Walker

Chu

1992

J. Clin. Invest.

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The Na+,K+-ATPase ion pump plays a critical role in fluid and electrolyte physiology of the small intestine. Here we show that, of the three known a isotypes (al, a2, and a3) of the sodium pump found in the rat, only al is expressed in the small intestine. The expression of this isotype, considered at the level of mRNA, is under developmental control, with the adult intestine exhibiting approximately a threefold increase in al message over the neonate. Cortisone treatment of the neonate results in near-adult levels of al mRNA expression. An increase in the abundance of al isotype parallels the changes in its mRNA expression. ,B subunit mRNA is expressed coordinately with the al subunit mRNA. A four-to five-fold rise in the Na+,K+-ATPase activity is also developmentally induced. (J.

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Section: Discussionmentioning

confidence: 76%

Expression and developmental regulation of Na+,K+ adenosine triphosphatase in the rat small intestine.

Zemelman¹,

Walker

Chu

1992

J. Clin. Invest.

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“…POSTENTERITIS SYNDROME-GROUP 2 Comparison of the enzyme activities of patients in the recovery phase with those in the active phase (Table 2) reveals a significant increase in (Na'-K')-ATPase, percentage of activation and basal activity of adenylate cyclase. In four patients where serial biopsies were taken during both the active and the recover phases (Fig.…”

Section: Toddler Diarrheamentioning

confidence: 99%

“…However, glucocorticoid administration to rats has been shown to stimulate (Na'-K')-ATPase activity to a degree that reverses secretion-induced by cholera toxin (2). Thus, it is conceivable that in certain situations increased (Nat-K')-ATPase activity might represent a compensatory mechanism to counteract the action of secretagogues.…”

Section: Toddler Diarrheamentioning

confidence: 99%

Mucosal (Na+-K+)-ATPase and Adenylate Cyclase Activities in Children with Toddler Diarrhea and the Postenteritis Syndrome

1980

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Summaryperformed to exclude asymptomatic coeliac disease and were normal under light microscopy. Full investigations including heAssays for (Na+-K+)-ATPase and fluoride moglobin, white cell count, differential, erythrocyte sedimentation and percentage of activation of adeny'ate cyclase have been rate, microscopy, culture of urine, plasma electrolytes, urea, calestablished for small portions of human jejunal biopsies. Control cium, magnesium, phosphate, proteins, transambases, alkaline means and ranges have been established for each activity in a phosphatase, immunoglobulins, urinary vanillin mandelin acid, group of children with failure to thrive but no gastrointestinal amino acids, sweat tests and, where indicated, barium disease. Activities of (Na+-K+)-ATPase and percentage of acti-contrast studies were all within normal limits. None were hypovation and basal lctivity of aden~late c~clase are increased in thyroid or had growth hormone deficiency by standard criteria.children with toddler diarrhea. (Na+-K+)-ATPase activity is reduced in children with active postenteritis syndrome, and recovery from this syndrome is associated with an increase in this activity and of percentage of activation and basal activity of adenylate cyclase.

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“…After 3 h, both jejunal loops were cannulated and washed with 100 ml of warm PBS during a 20-min period. Water transport was then determined in vivo by the single pass perfusion technique using the nonabsorbable marker, PEG as previously described (10). Loops were perfused at a constant temperature (37°C), and rate (0.5 ml/min) with a peristaltic pump (model 1203; Harvard Apparatus Co., Millis, MA) while maintaining body temperature at 37°C with a thermocouple controlled heating lamp.…”

Section: Methodsmentioning

confidence: 99%

Pathogenesis of Shigella diarrhea. XVI. Selective targetting of Shiga toxin to villus cells of rabbit jejunum explains the effect of the toxin on intestinal electrolyte transport.

et al. 1989

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To examine the mechanism by which Shiga toxin alters intestinal water and electrolyte transport, ligated loops of rabbit jejunum were incubated in vivo with purified toxin and then studied in vivo by single pass perfusion and in vitro by the Ussing chamber voltage-clamp technique. Toxin exposure led to accumulation of water in the jejunal lumen, associated with decreased active basal NaCi absorption. Glucose-and alaninestimulated Na absorption were also reduced, while toxin had no effect on either basal short-circuit current or the secretory response to theophylline. These observations suggest that Shiga toxin selectively inhibits NaCl absorption without significantly altering active anion secretion. To localize the cellular site of toxin action, populations of villus and crypt cells from rabbit jejunum were isolated and studied. Villus cells had a greater content of the glycolipid Shiga toxin receptor, Gb3, had more toxin binding sites than did crypt cells, and were much more sensitive than crypt cells to toxin-induced inhibition of protein synthesis. These experiments demonstrate that purified Shiga toxin inhibits jejunal fluid absorption .without affecting active fluid secretion by a preferential effect on villus cells. The results suggest that this is due to the differential distribution of toxin receptors on villus compared to crypt cells.

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

Cited by 71 publications

References 22 publications

Expression and developmental regulation of Na+,K+ adenosine triphosphatase in the rat small intestine.

Expression and developmental regulation of Na+,K+ adenosine triphosphatase in the rat small intestine.

Mucosal (Na+-K+)-ATPase and Adenylate Cyclase Activities in Children with Toddler Diarrhea and the Postenteritis Syndrome

Pathogenesis of Shigella diarrhea. XVI. Selective targetting of Shiga toxin to villus cells of rabbit jejunum explains the effect of the toxin on intestinal electrolyte transport.

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