Stimulatory Effects of 5-Hydroxytryptamine on Fluid Secretion and Transmural Potential Difference in Rat Small Intestine are Mediated by Different Receptor Subtypes

1990 ◽  
Vol 42 (1) ◽  
pp. 35-39 ◽  
Author(s):  
E. Beubler ◽  
I. M. Coupar ◽  
J. Hardcastle ◽  
P. T. Hardcastle
Keyword(s):  
Small Intestine ◽  
Fluid Secretion ◽  
Potential Difference ◽  
Receptor Subtypes ◽  
Rat Small Intestine

Role of 5-HT in cholera toxin-induced mucin secretion in the rat small intestine

1996 ◽  
Vol 270 (6) ◽  
pp. G1001-G1009 ◽  
Author(s):  
B. A. Moore ◽  
K. A. Sharkey ◽  
M. Mantle
Keyword(s):  
Small Intestine ◽  
Receptor Antagonist ◽  
Cholera Toxin ◽  
Receptor Subtypes ◽  
Rat Small Intestine ◽  
Mucin Secretion ◽  
Common Pathway ◽  
Distal Small Intestine ◽  
Intestinal Segments

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.

Distribution of Muscarinic Receptor Subtypes in Rat Small Intestine

1998 ◽  
Vol 80 (2) ◽  
pp. 320-325 ◽  
Author(s):  
Andreas M. Stadelmann ◽  
Susan Walgenbach-Telford ◽  
Gordon L. Telford ◽  
Timothy R. Koch
Keyword(s):  
Small Intestine ◽  
Muscarinic Receptor ◽  
Receptor Subtypes ◽  
Rat Small Intestine ◽  
Muscarinic Receptor Subtypes

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

1993 ◽  
Vol 105 (5) ◽  
pp. 1286-1293 ◽  
Author(s):  
Mats Jodal ◽  
Susanne Holmgren ◽  
Ove Lundgren ◽  
Anders Sjöqvist
Keyword(s):  
Small Intestine ◽  
Cholera Toxin ◽  
Myenteric Plexus ◽  
Fluid Secretion ◽  
Rat Small Intestine

Expression and effects of metabotropic CRF1 and CRF2 receptors in rat small intestine

2005 ◽  
Vol 288 (5) ◽  
pp. G1091-G1103 ◽  
Author(s):  
Christophe Porcher ◽  
Aurélie Juhem ◽  
André Peinnequin ◽  
Valérie Sinniger ◽  
Bruno Bonaz
Keyword(s):  
Small Intestine ◽  
Neural Control ◽  
Contractile Activity ◽  
Circular Muscle ◽  
Nerve Fibers ◽  
Receptor Subtypes ◽  
Rat Small Intestine ◽  
Duodenal Motility ◽  
Functional Studies

Corticotropin-releasing factor (CRF)-like peptides mediate their effects via two receptor subtypes, CRF1 and CRF2; these receptors have functional implication in the motility of the stomach and colon in rats. We evaluated expression and functions of CRF1 and CRF2 receptors in the rat small intestine (i.e., duodenum and ileum). CRF1–2-like immunoreactivity (CRF1–2-LI) was localized in fibers and neurons of the myenteric and submucosal ganglia. CRF1–2-LI was found in nerve fibers of the longitudinal and circular muscle layers, in the mucosa, and in mucosal cells. Quantitative RT-PCR showed a stronger expression of CRF2 than CRF1 in the ileum, whereas CRF1 expression was higher than CRF2 expression in the duodenum. Functional studies showed that CRF-like peptides increased duodenal phasic contractions and reduced ileal contractions. CRF1 antagonists (CP-154,526 and SSR125543Q) blocked CRF-like peptide-induced activation of duodenal motility but did not block CRF-like peptide-induced inhibition of ileal motility. In contrast, a CRF2 inhibitor (astressin2-B) blocked the effects of CRF-like peptides on ileal muscle contractions but did not influence CRF-like peptide-induced activation of duodenal motility. These results demonstrate the presence of CRF1–2 in the intestine and demonstrate that, in vitro, CRF-like peptides stimulate the contractile activity of the duodenum through CRF1 receptor while inhibiting phasic contractions of the ileum through CRF2 receptor. These results strongly suggest that CRF-like peptides play a major role in the regulatory mechanisms that underlie the neural control of small intestinal motility through CRF receptors.

scholarly journals Abatement of Forskolin-induced Intestinal Fluid Secretion by Modulation of Intracellular Camp With Penicillin

2021 ◽  
Author(s):  
Earnest Chen ◽  
Jason L. Own ◽  
Jenna Ollodart ◽  
Zeren Toksoy ◽  
Bruce A. Davis ◽  
...  
Keyword(s):  
Small Intestine ◽  
Gut Microbiome ◽  
Fluid Secretion ◽  
The Elderly ◽  
Penicillin G ◽  
Intracellular Camp ◽  
Protective Effects ◽  
Rat Small Intestine ◽  
Intestinal Fluid ◽  
Electrolyte Secretion

Abstract Millions of people die every year due to diarrheal related diseases, with infants and the elderly making up the majority of these deaths. Deaths are caused by excessive intestinal fluid and electrolyte secretion and are especially common in impoverished developing countries. Antibiotics have been classically used as a method to treat diarrhea-related pathologies by modulating the gut microbiome. We recently reported that penicillin may protect against disease-induced excessive fluid and electrolyte secretion via a genetics-independent, microbiome-independent mechanism in individual colonic crypt cells. In this study we investigated whether microbial-independent protective effects of penicillin against fluid secretion can be observed in the rat small intestine at the whole-tissue level. Here we report that penicillin has a significant dose-dependent protective effect against fluid secretion in induced models of diarrhea in the microbiome deficient rat small intestine. Penicillin can rapidly bring fluid secretion down to levels comparable to healthy controls. Our results suggest, for the first time, an alternative function for penicillin G as a cost-effective and fast-acting treatment against diarrheal symptoms without dependence on modulating the behavior of the existing gut microbiome.

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