Effect of Bicarbonate, Acetate, and Citrate on Water and Sodium Movement in Normal and Cholera Toxin-Treated Rat Small Intestine

We examined the role of 5-hydroxytryptamine (5-HT) in cholera toxin (CT)-induced mucin secretion in the proximal and distal regions of the rat small intestine. Neither the 5-HT2 receptor antagonist ketanserin nor the cyclooxygenase inhibitor indomethacin was capable of inhibiting choleraic mucin secretion. However, in the presence of the mixed 5-HT3/4 receptor antagonist tropisetron at doses that block both receptor subtypes, the secretory response was reduced to baseline levels in the proximal and distal small intestine. The selective 5-HT3 receptor antagonist ondansetron had no significant effect. These findings suggest that choleraic mucin secretion is mediated primarily through the activation of a 5-HT4-like receptor. Mucin secretion in response to the exogenous application of 5-HT occurs via two pathways: one is mediated by a 5-HT4-like receptor and is capsaicin sensitive but tetrodotoxin (TTX) insensitive, and one lacks the capsaicin-sensitive 5-HT4-mediated response but is TTX sensitive. Both converge on a common pathway that is cholinergic. No significant differences were observed between proximal and distal intestinal segments.

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Developmental differences in the expression of the cholera toxin sensitive subunit (Gs alpha) of adenylate cyclase in the rat small intestine.

Gut ◽

10.1136/gut.38.6.853 ◽

1996 ◽

Vol 38 (6) ◽

pp. 853-858 ◽

Cited By ~ 6

Author(s):

I R Sanderson ◽

Z Xu ◽

S W Chu ◽

Q Y Xie ◽

L J Levine ◽

...

Keyword(s):

Small Intestine ◽

Adenylate Cyclase ◽

Cholera Toxin ◽

Developmental Differences ◽

Rat Small Intestine ◽

Gs Alpha

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Neural mediation of cholera toxin-induced mucin secretion in the rat small intestine

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1993.265.6.g1050 ◽

1993 ◽

Vol 265 (6) ◽

pp. G1050-G1056 ◽

Cited By ~ 6

Author(s):

B. A. Moore ◽

K. A. Sharkey ◽

M. Mantle

Keyword(s):

Small Intestine ◽

Cholera Toxin ◽

Fold Increase ◽

Open Loop ◽

Sensory Nerves ◽

Loop Model ◽

Rat Small Intestine ◽

Mucin Secretion ◽

Distal Small Intestine

We examined the role of enteric nerves in cholera toxin (CT)-induced mucin secretion in proximal and distal regions of rat small intestine. Stimulation of intestinal loops with 120 micrograms (1.5 mumol) CT using an in vitro open-loop model resulted in an approximately four-fold increase in luminal mucin content over unstimulated controls in both regions of the gut. Prior treatment of loops with tetrodotoxin had no effect on the amount of mucin released in response to CT. However, permanent destruction of primary sensory afferent nerves by neonatal treatment of rats with capsaicin reduced the mucin response to CT to baseline levels in both regions. In normal animals, atropine resulted in approximately 40% inhibition of mucin secretion in both the proximal and distal small intestine. The atropine-sensitive secretory response appears to be a component of the capsaicin-sensitive response. These results suggest that choleraic mucin secretion is mediated primarily by a capsaicin-sensitive neurogenic pathway involving local activation of sensory nerves, which may then elicit mucin secretion through interaction with cholinergic nerves.

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Involvement of the myenteric plexus in the cholera toxin-induced net fluid secretion in the rat small intestine

Gastroenterology ◽

10.1016/0016-5085(93)90130-5 ◽

1993 ◽

Vol 105 (5) ◽

pp. 1286-1293 ◽

Cited By ~ 59

Author(s):

Mats Jodal ◽

Susanne Holmgren ◽

Ove Lundgren ◽

Anders Sjöqvist

Keyword(s):

Small Intestine ◽

Cholera Toxin ◽

Myenteric Plexus ◽

Fluid Secretion ◽

Rat Small Intestine

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88 Absorption of Water From a Liposomal Oral Rehydration Solution: an In Vivo Perfusion Study of Rat Small Intestine Exposed to Cholera Toxin

Gastroenterology ◽

10.1016/s0016-5085(12)60083-3 ◽

2012 ◽

Vol 142 (5) ◽

pp. S-21

Author(s):

Pradip K. Bardhan ◽

Nasirul Islam ◽

Rifat Faruqui

Keyword(s):

Small Intestine ◽

Cholera Toxin ◽

Oral Rehydration Solution ◽

Rat Small Intestine ◽

Perfusion Study ◽

Oral Rehydration ◽

Rehydration Solution

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The effect of Escherichia coli STa enterotoxin and other secretagogues on mucosal surface pH of rat small intestine in vivo

Proceedings of the Royal Society of London Series B Biological Sciences ◽

10.1098/rspb.1988.0045 ◽

1988 ◽

Vol 234 (1275) ◽

pp. 219-237 ◽

Cited By ~ 55

Keyword(s):

Escherichia Coli ◽

Small Intestine ◽

Cyclic Amp ◽

Cholera Toxin ◽

Cyclic Gmp ◽

Mucosal Surface ◽

Jejunal Mucosa ◽

Rat Small Intestine ◽

Surface Ph

The mucosal surface pH of rat small intestine was measured in vivo . The surface pH in the normal jejunum was 6.20 ± 0.02 (67) and 7.00 ± 0.05 (5) in the ileum. Escherichia coli STa toxin induced a rapid and reversible alkalinization of both jejunal and ileal mucosae to a pH of 6.91 ± 0.08 (10) and 7.67 ± 0.06 (5) respectively. The synthetic ST analogue, STh-(6-19), had an effect identical to native STa toxin on jejunal surface pH. Theophylline (20 mM) maintained the STa-elevated jejunal surface pH after toxin removal but had no effect on untreated tissue. 8-Bromo cyclic GMP resembled STa by causing similar mucosal alkalinization in the jejunum; 8-bromo cyclic AMP, forskolin and cholera toxin individually had considerably smaller effects on surface pH, although combining forskolin or cholera toxin with theophylline resulted in alkalinization of the jejunal mucosa to a pH of 6.92 ± 0.03 (5) and 6.76 ± 0.04 (4). These results indicate that cyclic-GMP-dependent secretory processes are more capable of inducing surface pH changes than those dependent on cyclic AMP. The ability of STa to alter mucosal surface pH makes it a useful tool to investigate the microclimate hypothesis for weak electrolyte absorption.

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