The suppressant effect of GEA3162 on spontaneous serotonin release from human colonic mucosa in vitro

Kojima, Sunao; Uchida, Kohsuke; Sasaki, Kenji; Sunagawa, Masakatu; Ohno, Yasuo; Kamikawa, Yuichiro

doi:10.1016/j.ejphar.2006.08.047

Cited by 3 publications

(2 citation statements)

References 13 publications

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“…Regulation of 5-HT release from the colonic mucosa may lead to new ways to control defecation or constipation in diseases such as irritable bowel syndrome (IBS). GEA3162 can suppress the 5-HT release via an action on colonic mucosa through a mechanism independent of the ODQ-sensitive cyclic GMP system or peroxynitrite generation [73].…”

Section: 234-oxatriazolium-5-aminidesmentioning

confidence: 99%

The Chemistry of Bioactive Mesoionic Heterocycles

Kawase

Sakagami

Motohashi

2007

Topics in Heterocyclic Chemistry

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Section: 234-oxatriazolium-5-aminidesmentioning

confidence: 99%

The Chemistry of Bioactive Mesoionic Heterocycles

Kawase

Sakagami

Motohashi

2007

Topics in Heterocyclic Chemistry

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“…Kojima et al [46] demonstrated that a lipophilic nitric oxide (NO)-releasing compound 5-amino-3-(3, 4-dichlorophenyl) 1,2,3,4-oxatriazolium (GEA3162) can suppress 5-HT release from colonic mucosa through a mechanism that does not involve cyclic GMP system or peroxynitrite generation. The effects of this agent on 5-HT secretion in response to infection have not been reported to date.…”

Section: Novel Treatment Strategies Targeting Enteroendocrine and Neumentioning

confidence: 99%

Enteroendocrine and Neuronal Mechanisms in Pathophysiology of Acute Infectious Diarrhea

2011

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Background While enterocyte secretion is the predominant mechanism considered responsible for secretory diarrhea in response to acute enteric infections, there are several lines of evidence that support alternative mechanisms controlling fluid and electrolyte secretion in diarrhea. Aim To review enteroendocrine and neuronal mechanisms that participate in the development of acute infectious diarrhea. Recent Advances Acute infectious diarrheas due to bacterial toxins (e.g., cholera, E. coli heat-stable enterotoxin, C. difficile) and rotavirus are all associated with secretion of transmitters from enteroendocrine cells (e.g., 5-HT) and activation of afferent neurons that stimulate submucosal secretomotor neurons. The latter secrete acetylcholine (which binds to muscarinic receptors on epithelial cells) and VIP. Involvement of nerves was demonstrated by inhibition of bacterial toxin-induced secretion by hexamethonium (nicotinic), tetrodotoxin (Na+ channel blocker), and lidocaine (visceral/mucosal afferents). Nicotinic receptors are present on secretomotoneurons and these are activated by release of acetylcholine from enteric interneurons or extrinsic efferent fibers. Specific organisms also modify other mechanisms that may contribute to development of acute diarrhea. Thus, mucin secretion, activation of motor mechanisms, increased mucosal permeability and inhibition of bile acid absorption have been reported in specific types of acute infectious diarrhea. Conclusion New therapies targeting neural and transmitter mediation including 5-HT, VIP, NPY, as well as toxin receptors and channels activated during acute infectious diarrhea could usher in a novel approach to enhancing glucose–electrolyte solutions used in the treatment of acute diarrhea.

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Oxatriazoles

Fraser

2008

Comprehensive Heterocyclic Chemistry III

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The suppressant effect of GEA3162 on spontaneous serotonin release from human colonic mucosa in vitro

Cited by 3 publications

References 13 publications

The Chemistry of Bioactive Mesoionic Heterocycles

The Chemistry of Bioactive Mesoionic Heterocycles

Enteroendocrine and Neuronal Mechanisms in Pathophysiology of Acute Infectious Diarrhea

Oxatriazoles

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