Stimulation of duodenal HCO<sub>3</sub><sup>−</sup> secretion by hydrogen sulphide in rats: relation to prostaglandins, nitric oxide and sensory neurones

Ise, Fumitaka; Takasuka, Hironori; Hayashi, Satoru; Takahashi, Kazuaki; Koyama, Masafumi; Aihara, Eitaro; Takeuchi, Koji

doi:10.1111/j.1748-1716.2010.02152.x

Cited by 39 publications

(31 citation statements)

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“…Furthermore, CO stimulates epithelial Cl Ϫ secretion in the intestine (Uc et al, 2005). We have reported that hydrogen sulfide, generated endogenously in the mammalian body and recognized as a gaseous signaling molecule, is involved in the mechanism regulating acidinduced duodenal HCO 3 Ϫ secretion (Ise et al, 2011). These findings suggest that CO also plays a role in the physiology of the gastrointestinal tract, yet it remains unclear whether endogenous CO participates in the regulation of duodenal HCO 3 Ϫ secretion.…”

Section: Introductionmentioning

confidence: 79%

“…An accumulative body of evidence suggests that CO functions as a gaseous signaling molecule in the body, in addition to NO and hydrogen sulfide, and acts as a vasodilator or neuromodulators (Moncada et al, 1991;Maines, 1997;Abraham and Kappas, 2008;Linden et al, 2008;Ise et al, 2011). Studies have also showed the physiological and pathophysiological roles of CO in the gastrointestinal tract (Gibbons and Farrugia, 2004); CO causes relaxation in the stomach fundus and the jejunum via the activation of soluble guanylate cyclase and K ϩ channels (De Backer and Lefebvre, 2007).…”

Section: Discussionmentioning

confidence: 99%

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Carbon Monoxide Involved in Modulating HCO₃⁻ Secretion in Rat Duodenum

Takasuka

Hayashi²,

Koyama³

et al. 2011

J Pharmacol Exp Ther

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We examined the effect of the tricarbonyl-dichlororuthenium (II) dimer (CORM-2), a carbon monoxide (CO) donor, on duodenal HCO 3 Ϫ secretion in rats and investigated whether endogenous CO produced by heme oxygenase (HO) is involved in the regulation of this secretion. Under urethane anesthesia, a duodenal loop was perfused with saline, and HCO 3 Ϫ secretion was measured at pH 7.0 using a pH stat method. CORM-2, biliverdin, FeCl 2 , or ruthenium (III) chloride hydrate (RuCl 3 ) was applied to the loop for 5 min. The mucosal application of CORM-2 dose-dependently increased HCO 3 Ϫ secretion, whereas neither RuCl 3 , FeCl 2 , nor biliverdin had an effect. The stimulatory effect was significantly attenuated by indomethacin but not N G -nitro-L-arginine methyl ester. The application of CORM-2 increased the mucosal prostaglandin (PG) E 2 content of the duodenum. The acid-induced HCO 3 Ϫ response was markedly inhibited by indomethacin and Sn(IV) protoporphyrin IX dichloride (SnPP; an inhibitor of HO) but not Cu(II) protoporphyrin dichloride, and the inhibitory effect of SnPP was significantly reversed by pretreatment with hemin, a substrate of HO. Perfusion of the duodenal loop with 100 mM HCl for 2 h caused a few hemorrhagic lesions in the mucosa, and this response was significantly worsened by the prior administration of SnPP and indomethacin. The expression of HO-1 but not HO-2 protein was up-regulated in the duodenum after the acid treatment. These results suggest that CO, generated endogenously or exogenously, stimulates HCO 3 Ϫ secretion in the duodenum, and this effect is mediated by endogenous PGs. It is assumed that HO/CO plays a role in maintaining the integrity of the duodenal mucosa.

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Section: Introductionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide Involved in Modulating HCO₃⁻ Secretion in Rat Duodenum

Takasuka

Hayashi²,

Koyama³

et al. 2011

J Pharmacol Exp Ther

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“…H 2 S also influences nonvascular factors that contribute to mucosal defense. For instance, it can stimulate duodenal bicarbonate secretion (30), which helps to protect the stomach and small intestine from the damaging effects of gastric acid. As mentioned above, H 2 S can be utilized by mitochondria to generate ATP, particularly in settings of hypoxia (27,36).…”

Section: G469 Hydrogen Sulfide-based Therapeuticsmentioning

confidence: 99%

Hydrogen sulfide-based therapeutics and gastrointestinal diseases: translating physiology to treatments

Chan

Wallace

2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…H 2 S mediates anti-inflammatory roles in the digestive tract and is protective against ischemic damage (47,50,107) and ethanol-induced gastritis (52). The gasotransmitter stimulates bicarbonate secretion, which aids in the defense of the mucosa of the stomach and small intestine against gastric acid (32). Accordingly, H 2 S-releasing nonsteroidal anti-inflammatory drugs have been developed (13).…”

Section: Introductionmentioning

confidence: 99%

Modes of Physiologic H₂S Signaling in the Brain and Peripheral Tissues

Paul

Snyder²

2015

Antioxidants & Redox Signaling

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Significance: Hydrogen sulfide (H 2 S), once associated with rotten eggs and sewers, is now recognized as a gasotransmitter that is synthesized in vivo in a regulated fashion. This ancient gaseous molecule has been retained throughout evolution to perform various roles in different life forms. H 2 S modulates important signaling functions in diverse cellular processes ranging from regulation of blood pressure to redox homeostasis. Recent Advances: One of the modes by which H 2 S signals is by post-translational modification of reactive cysteine residues in a process designated as sulfhydration, resulting in conversion of the -SH groups of target cysteine residues to -SSH. Using the modified biotin-switch assay and a fluorescent maleimide-based analysis, sulfhydration of several proteins has been detected in various cell types. Aberrant sulfhydration patterns occur in neurodegenerative conditions such as Parkinson's disease. Critical Issues: The exact concentration, source of H 2 S, and conditions under which various stores of H 2 S are utilized have not been fully elucidated. Currently, available inhibitors of the biosynthetic enzymes of H 2 S lack sufficient specificity to shed light on detailed mechanisms of H 2 S action. Probes with a higher sensitivity that can reliably detect cellular and tissue H 2 S levels are yet to be developed. Future Directions: Availability of advanced probes and biosynthesis inhibitors would help in the measurement of real-time changes of endogenous H 2 S levels in an in vivo context. The study of the dynamics of sulfhydration and nitrosylation of critical cysteine residues of regulatory proteins involved in physiology and pathophysiology is an area of interest for the future. Antioxid. Redox Signal. 22,[411][412][413][414][415][416][417][418][419][420][421][422][423]

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Stimulation of duodenal HCO₃⁻ secretion by hydrogen sulphide in rats: relation to prostaglandins, nitric oxide and sensory neurones

Cited by 39 publications

References 41 publications

Carbon Monoxide Involved in Modulating HCO₃⁻ Secretion in Rat Duodenum

Carbon Monoxide Involved in Modulating HCO₃⁻ Secretion in Rat Duodenum

Hydrogen sulfide-based therapeutics and gastrointestinal diseases: translating physiology to treatments

Modes of Physiologic H₂S Signaling in the Brain and Peripheral Tissues

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Stimulation of duodenal HCO3− secretion by hydrogen sulphide in rats: relation to prostaglandins, nitric oxide and sensory neurones

Cited by 39 publications

References 41 publications

Carbon Monoxide Involved in Modulating HCO3− Secretion in Rat Duodenum

Carbon Monoxide Involved in Modulating HCO3− Secretion in Rat Duodenum

Hydrogen sulfide-based therapeutics and gastrointestinal diseases: translating physiology to treatments

Modes of Physiologic H2S Signaling in the Brain and Peripheral Tissues

Contact Info

Product

Resources

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Stimulation of duodenal HCO₃⁻ secretion by hydrogen sulphide in rats: relation to prostaglandins, nitric oxide and sensory neurones

Carbon Monoxide Involved in Modulating HCO₃⁻ Secretion in Rat Duodenum

Carbon Monoxide Involved in Modulating HCO₃⁻ Secretion in Rat Duodenum

Modes of Physiologic H₂S Signaling in the Brain and Peripheral Tissues