Nitrergic Pathway Is the Main Contributing Mechanism in the Human Gastric Fundus Relaxation: An In Vitro Study

Ye, Min; Hong, Yun Soo; Ko, Eun-Ju; Lee, Ji-Yeon; Ahn, Ki Duck; Bae, Je Moon; Rhee, Poong–Lyul

doi:10.1371/journal.pone.0162146

Cited by 14 publications

(11 citation statements)

References 30 publications

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“…Preincubation of the gastric muscle with L‐NNA did not significantly alter its contraction parameters; therefore, NO does not appear to be tonically active in the gastric fundus, which is consistent with the observation of Holzer‐Petsche and Moser 48 . However, other researchers observed increases in amplitude and basal tension after incubation with L‐NNA 49,50 . In turn, L‐NAME significantly inhibited contractility induced by carbachol.…”

Section: Discussionsupporting

confidence: 87%

Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway

Modzelewska

Drygalski

Kleszczewski

et al. 2021

Neurogastroenterology Motil

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Background: Quercetin has recently become a remarkably popular subject of research due to its broad beneficial pharmacological properties. The goal of our study was to observe its effects on contractility of human gastric smooth muscles in reference to the NO pathway and direct influence of potassium channels.Methods: Tissues were obtained from patients undergoing sleeve gastrectomy due to morbid obesity (n = 10 aged 24-56; BMI 47.16 ± 1.84). The following parameters were evaluated in the recordings: area under the curve (AUC), average baseline muscle tone, and relative change in muscle contraction. Key Results: Quercetin induced noticeable, dose-dependent relaxation of the carbachol treated gastric strips. The substantial effect was noted at concentrations higher than 10 −7 mol/L and maximal at 10 −4 mol/L (81.82 ± 3.32%; n = 10; p < 0.0001) of the control.Neither NOS blockers nor guanylyl cyclase blockers had inhibitory effects on the relaxation of strips induced by examined polyphenol. Glibenclamide inhibited the relaxing effect of quercetin, significant at concentrations higher than 5⋅10 −5 mol/L. Preincubation with charybdotoxin or apamin extended the relaxing effect of quercetin (from 10 −6 mol/L).Tamoxifen, in turn, significantly increased muscle relaxation at all quercetin concentrations. Conclusions & Inferences:In conclusion, the current study was the first to show that quercetin-induced relaxation of human gastric smooth muscle occurs directly through K + ATP channels and independently to NO pathways. The present results suggest that quercetin is a potential nutraceutical in the treatment of functional gastrointestinal dyspepsia and other minor gastric muscle motility disturbance.

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Section: Discussionsupporting

confidence: 87%

Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway

Modzelewska

Drygalski

Kleszczewski

et al. 2021

Neurogastroenterology Motil

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“…Thus, the reduction in amplitude of the neurally-induced contractile responses by ADPN, observed in the present experiments, may be ascribable to either a minor activation of the excitatory component or to a major nervous inhibitory influence exerted on the smooth muscle. In this view, NO is considered the main NANC inhibitory neurotransmitter released during EFS to cause gastrointestinal relaxation[ 19 , 20 ]. Actually, the increase in amplitude of the EFS-induced contractile responses by the NO synthesis inhibitor L-NNA supports the removal of a nitrergic inhibitory nervous influence.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin affects the mechanical responses in strips from the mouse gastric fundus

Idrizaj

Garella

Castellini

et al. 2018

WJG

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AIMTo investigate whether the adipocytes derived hormone adiponectin (ADPN) affects the mechanical responses in strips from the mouse gastric fundus.METHODSFor functional experiments, gastric strips from the fundal region were cut in the direction of the longitudinal muscle layer and placed in organ baths containing Krebs-Henseleit solution. Mechanical responses were recorded via force-displacement transducers, which were coupled to a polygraph for continuous recording of isometric tension. Electrical field stimulation (EFS) was applied via two platinum wire rings through which the preparation was threaded. The effects of ADPN were investigated on the neurally-induced contractile and relaxant responses elicited by EFS. The expression of ADPN receptors, Adipo-R1 and Adipo-R2, was also evaluated by touchdown-PCR analysis.RESULTSIn the functional experiments, EFS (4-16 Hz) elicited tetrodotoxin (TTX)-sensitive contractile responses. Addition of ADPN to the bath medium caused a reduction in amplitude of the neurally-induced contractile responses (P < 0.05). The effects of ADPN were no longer observed in the presence of the nitric oxide (NO) synthesis inhibitor L-NG-nitro arginine (L-NNA) (P > 0.05). The direct smooth muscle response to methacholine was not influenced by ADPN (P > 0.05). In carbachol precontracted strips and in the presence of guanethidine, EFS induced relaxant responses. Addition of ADPN to the bath medium, other than causing a slight and progressive decay of the basal tension, increased the amplitude of the neurally-induced relaxant responses (P < 0.05). Touchdown-PCR analysis revealed the expression of both Adipo-R1 and Adipo-R2 in the gastric fundus.CONCLUSIONThe results indicate for the first time that ADPN is able to influence the mechanical responses in strips from the mouse gastric fundus.

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“…The regulatory part of the GIVC includes vagal afferents and second‐order neurons in the NTS for vagovagal reflex and other neurons that provide input to the NTS neurons. Esophagogastric relaxation and gastric accommodation reflexes are well‐studied gastric inhibitory vagovagal reflexes . The vagal afferents have their cell bodies in the nodose ganglion.…”

Section: Gastric Inhibitory Vagal Motor Circuit (Givmc)mentioning

confidence: 99%

“…Esophagogastric relaxation and gastric accommodation reflexes are well-studied gastric inhibitory vagovagal reflexes. 40,[52][53][54] The vagal afferents have their cell bodies in the nodose ganglion. Originally, neural input to the DMV-C-i was thought to be from vagal afferents leading to monosynaptic vagovagal reflexes.…”

Section: G a S Tri C Inhib Itory Vag Al Motor Circu It (G Ivm C)mentioning

confidence: 99%

Advances in the physiology of gastric emptying

Goyal

Guo

Mashimo

2019

Neurogastroenterology Motil

235

154

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There have been many recent advances in the understanding of various aspects of the physiology of gastric motility and gastric emptying. Earlier studies had discovered the remarkable ability of the stomach to regulate the timing and rate of emptying of ingested food constituents and the underlying motor activity. Recent studies have shown that two parallel neural circuits, the gastric inhibitory vagal motor circuit (GIVMC) and the gastric excitatory vagal motor circuit (GEVMC), mediate gastric inhibition and excitation and therefore the rate of gastric emptying. The GIVMC includes preganglionic cholinergic neurons in the DMV and the postganglionic inhibitory neurons in the myenteric plexus that act by releasing nitric oxide, ATP, and peptide VIP. The GEVMC includes distinct gastric excitatory preganglionic cholinergic neurons in the DMV and postganglionic excitatory cholinergic neurons in the myenteric plexus. Smooth muscle is the final target of these circuits. The role of the intramuscular interstitial cells of Cajal in neuromuscular transmission remains debatable. The two motor circuits are differentially regulated by different sets of neurons in the NTS and vagal afferents. In the digestive period, many hormones including cholecystokinin and GLP‐1 inhibit gastric emptying via the GIVMC, and in the inter‐digestive period, hormones ghrelin and motilin hasten gastric emptying by stimulating the GEVMC. The GIVMC and GEVMC are also connected to anorexigenic and orexigenic neural pathways, respectively. Identification of the control circuits of gastric emptying may provide better delineation of the pathophysiology of abnormal gastric emptying and its relationship to satiety signals and food intake.

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Nitrergic Pathway Is the Main Contributing Mechanism in the Human Gastric Fundus Relaxation: An In Vitro Study

Cited by 14 publications

References 30 publications

Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway

Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway

Adiponectin affects the mechanical responses in strips from the mouse gastric fundus

Advances in the physiology of gastric emptying

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