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Gas mediators involved in modulating duodenal HCO3(-) secretion
K Takeuchi1, E Aihara, M Kimura
1Division of Pathological Sciences, Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto 607-8414, Japan. takeuchi@mb.kyoto-phu.ac.jp
Current Medicinal Chemistry
|February 4, 2012
Summary
Gas mediators like nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO) stimulate duodenal bicarbonate secretion. These mediators, along with prostaglandins, protect against acid-induced duodenal damage.
Area of Science:
- Gastroenterology
- Physiology
- Molecular Biology
Background:
- Duodenal bicarbonate secretion is crucial for mucosal protection against acid.
- Gas mediators, including nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO), are implicated in gastrointestinal physiology.
- The interplay between gas mediators, prostaglandins (PGs), and duodenal bicarbonate secretion in response to acidification requires further elucidation.
Purpose of the Study:
- To investigate the role of endogenous and exogenous NO, H2S, and CO in regulating duodenal bicarbonate secretion.
- To explore the mechanisms by which these gas mediators influence duodenal bicarbonate secretion, including their interaction with prostaglandins and sensory neurons.
- To assess the protective effects of these gas mediators against acid-induced duodenal damage.
Main Methods:
- Measurement of duodenal bicarbonate secretion in response to mucosal acidification and administration of gas donor compounds (NOR3 for NO, NaHS for H2S, CORM-2 for CO).
- Assessment of the effects of inhibitors (indomethacin, L-NAME, propargylglycine, SnPP) and sensory deafferentation on bicarbonate secretion.
- Quantification of prostaglandin E2 (PGE2) production and luminal NO release.
- Evaluation of acid-induced duodenal damage in the presence or absence of gas mediator production.
Main Results:
- Exogenous NO, H2S, and CO donors stimulated duodenal bicarbonate secretion.
- The stimulatory effects of NO and CO were partly mediated by prostaglandins, while H2S involved prostaglandins, NO, and sensory neurons.
- Inhibition of endogenous PG, H2S, or CO production exacerbated acid-induced duodenal damage.
Conclusions:
- NO, H2S, and CO act as signaling molecules that stimulate duodenal bicarbonate secretion.
- These gas mediators, along with PGs, play a significant role in the local regulation of duodenal bicarbonate secretion and protection against acid injury.
- The findings highlight the importance of these gas mediators in maintaining duodenal mucosal integrity.
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