The Inhibitory Effects of Hydrogen Sulfide on Pacemaker Activity of Interstitial Cells of Cajal from Mouse Small Intestine

Parajuli, Shankar P.; Choi, Seok; Lee, Jun; Park, Chan Guk; Kim, Man Yoo; Kim, Hyun Il; Yeum, Cheol Ho; Jun, Jae Yeoul

doi:10.4196/kjpp.2010.14.2.83

Cited by 32 publications

(29 citation statements)

References 23 publications

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“…Low-dose activation of guinea-pig gastric smooth muscle may be mediated via inhibition of voltage-gated K + channels and high-dose inhibition may be mediated via K ATP channel activation (Zhao et al, 2009). In the mouse intestine, H 2 S inhibits pacemaker amplitude and frequency of interstitial cells of Cajal at high concentrations (0.5-1.0mmoll -1 ), but may slightly stimulate at low concentrations (50-100mmoll -1 ); these effects appear to be via modulation of intracellular calcium (Parajuli et al, 2010). H 2 S also stimulates proliferation of interstitial cells of Cajal (Huang et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Hydrogen sulfide (H2S) and hypoxia inhibit salmonid gastrointestinal motility: evidence for H2S as an oxygen sensor

Dombkowski

Naylor

Shoemaker

et al. 2011

Journal of Experimental Biology

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SUMMARYHydrogen sulfide (H 2 S) has been shown to affect gastrointestinal (GI) motility and signaling in mammals and O 2 -dependent H 2 S metabolism has been proposed to serve as an O 2 ʻsensorʼ that couples hypoxic stimuli to effector responses in a variety of other O 2 -sensing tissues. The low P O2 values and high H 2 S concentrations routinely encountered in the GI tract suggest that H 2 S might also be involved in hypoxic responses in these tissues. In the present study we examined the effect of H 2 S on stomach, esophagus, gallbladder and intestinal motility in the rainbow trout (Oncorhynchus mykiss) and coho salmon (Oncorhynchus kisutch) and we evaluated the potential for H 2 S in oxygen sensing by examining GI responses to hypoxia in the presence of known inhibitors of H 2 S biosynthesis and by adding the sulfide donor cysteine (Cys). We also measured H 2 S production by intestinal tissue in real time and in the presence and absence of oxygen. In tissues exhibiting spontaneous contractions, H 2 S inhibited contraction magnitude (area under the curve and amplitude) and frequency, and in all tissues it reduced baseline tension in a concentration-dependent relationship. Longitudinal intestinal smooth muscle was significantly more sensitive to H 2 S than other tissues, exhibiting significant inhibitory responses at 1-10mmoll -1 H 2 S. The effects of hypoxia were essentially identical to those of H 2 S in longitudinal and circular intestinal smooth muscle; of special note was a unique transient stimulatory effect upon application of both hypoxia and H 2 S. Inhibitors of enzymes implicated in H 2 S biosynthesis (cystathionine -synthase and cystathionine -lyase) partially inhibited the effects of hypoxia whereas the hypoxic effects were augmented by the sulfide donor Cys. Furthermore, tissue production of H 2 S was inversely related to O 2 ; addition of Cys to intestinal tissue homogenate stimulated H 2 S production when the tissue was gassed with 100% nitrogen (~0% O 2 ), whereas addition of oxygen (~10% O 2 ) reversed this to net H 2 S consumption. This study shows that the inhibitory effects of H 2 S on the GI tract of a non-mammalian vertebrate are identical to those reported in mammals and they provide further evidence that H 2 S is a key mediator of the hypoxic response in a variety of O 2 -sensitive tissues.

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Section: Introductionmentioning

confidence: 99%

“…Based on the responses at 100, 500 and 1000mmoll -1 (Nagao et al, 2010), the EC 50 appears to be ~500mmoll -1 . Similarly high concentrations (500mmoll -1 H 2 S) were necessary to affect pacemaker currents in interstitial cells of Cajal from mouse small intestine (Parajuli et al, 2010).…”

Section: Comparison Of H 2 S Effects In Mammals and Troutmentioning

confidence: 99%

Hydrogen sulfide (H2S) and hypoxia inhibit salmonid gastrointestinal motility: evidence for H2S as an oxygen sensor

Dombkowski

Naylor

Shoemaker

et al. 2011

Journal of Experimental Biology

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“…Western blotting results also demonstrated that both CBS and CSE were expressed in the rat and mouse stomach, and H2S synthesis in the rat stomach was about 75 nmol/g/h [25] . CBS and CSE were also identified in the small intestine [25][26][27][28][29][30] . In the rat duodenum and jejunum, both enzymes were expressed in the neurons of myenteric plexus, but not the smooth muscle cells or the interstitial cells of Cajal (ICCs) [27,29] .…”

Section: Ynthesis Of H2s In the Gastrointestinal Tractmentioning

confidence: 99%

“…Aside from enteric neurons and smooth muscle cells, as the pacemaker cells, the interstitial cell of Cajal (ICC) may be also a target of H2S to regulate the gastrointestinal motility. Albeit no expression of CBS or CSE in ICC, exogenous H2S was shown to inhibit the pacemaker activity of ICC [30] which may be partially responsible for the H2S-induced inhibition of small intestine motility.…”

Section: In the Stomachmentioning

confidence: 99%

“…However, it is not clear how H2S affect these channels. Recently, it has been well-established that H2S directly regulates the physiological functions by sulfhydrating a large number of cellular proteins [16] , for example, NaHS sulfhydrating sulfonylurea receptor 2B (SUR2B) subunit of KATP channel might partially interpret the effect of H2S on these channels; (3) H2S also can affect the pacemaker activity of ICC to modulate the smooth muscle motility [30] ; (4) As two of the important gaseous signal molecules, H2S and NO have interaction in regulating the gastrointestinal smooth muscle motility. They can cooperate with each other to relax the smooth muscle [46] , alternatively, they counteract each other to regulate the motility [24] .…”

Section: Mechanisms Of H2s In Regulating the Gastrointestinal Motilitymentioning

confidence: 99%

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Synthesis of H2S in the Gastrointestinal Tract

Huang

2015

Journal of Gastroenterology and Hepatology Research

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The transient receptor potential A1 ion channel (TRPA1) modifies in vivo autonomous ureter peristalsis in rats

Weinhold

Villa

Strittmatter

et al. 2020

Neurourology and Urodynamics

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Aims: The current study aimed to explore the expression of transient receptor potential A1 ion channels (TRPA1) in the rat ureter and to assess if TRPA1-active compounds modulate ureter function. Methods: The expression of TRPA1 in rat ureter tissue was studied by immunofluorescence. The TRPA1 distribution was compared to calcitonin generelated peptide (CGRP), α-actin (SMA1), anoctamin-1 (ANO1), and c-kit. For in vivo analyses, a catheter was implanted in the right ureter of 50 rats. Ureter peristalsis and pressures were continuously recorded by a data acquisition setup during intraluminal infusion of saline (baseline), saline plus protamine sulfate (PS; to disrupt the urothelium), saline plus PS with hydrogen sulfide (NaHS) or cinnamaldehyde (CA). Comparisons were made between rats treated systemically with vehicle or a TRPA1-antagonist (HC030031). Results: TRPA1-immunoreactive nerves co-expressed CGRP and were mainly located in the suburothelial region of the ureter. Immunoreactivity for TRPA1 was also encountered in c-kit-positive but ANO1-negative cells of the ureter suburothelium and wall. In vivo, HC030031-treated rats had elevated baseline peristaltic frequency (p < 0.05) and higher intraluminal pressures (p < 0.01). PS increased the frequency of ureter peristalsis versus baseline in vehicle-treated rats (p < 0.001) but not in HC030031-treated rats. CA (p < 0.001) and NaHS (p < 0.001) decreased ureter peristalsis. This was counteracted by HC030031 (p < 0.05 and p < 0.01). Conclusions: In rats, TRPA1 is expressed on cellular structures considered of importance for peristaltic and mechanoafferent functions of the ureter. Functional data indicate that TRPA1-mediated signals regulate ureter peristalsis. This effect was pronounced after mucosal disruption and suggests a role for TRPA1 in ureter pathologies involving urothelial damage.

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The Inhibitory Effects of Hydrogen Sulfide on Pacemaker Activity of Interstitial Cells of Cajal from Mouse Small Intestine

Cited by 32 publications

References 23 publications

Hydrogen sulfide (H2S) and hypoxia inhibit salmonid gastrointestinal motility: evidence for H2S as an oxygen sensor

Hydrogen sulfide (H2S) and hypoxia inhibit salmonid gastrointestinal motility: evidence for H2S as an oxygen sensor

Synthesis of H2S in the Gastrointestinal Tract

The transient receptor potential A1 ion channel (TRPA1) modifies in vivo autonomous ureter peristalsis in rats

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