The Role of Nitric Oxide in the Electrical Field Stimulation-Induced Contractions of Sphincter of Oddi and Gallbladder Strips in Guinea Pigs

Gültekin, Hülya; Erdem, Remzi; Emre-Aydıngöz, Selda; Tuncer, Meral

doi:10.1254/jphs.fp0060159

Cited by 8 publications

(5 citation statements)

References 18 publications

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“…CCK8 acts presynaptically within gallbladder ganglia to increase the release of acetylcholine from vagal terminals, [8,19] whereas nitric oxide, a primary gas messenger or nerve transmitter, serves as a potent and efficient relaxant of gallbladder smooth muscle in a manner similar to that in other smooth muscles. [20,21] In this study, we observed that MYPT1 also played essential functions in the contractile behaviors of the gallbladder. Deletion of MYPT1 led to dysfunctional motility of the gallbladder.…”

Section: Introductionmentioning

confidence: 67%

Gallbladder dysfunction caused by MYPT1 ablation triggers cholestasis-induced hepatic fibrosis in mice

Wang,

Jiang,

Zhou

et al. 2024

Hepatology Communications

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Background: The incidence of gallbladder diseases is as high as 20%, but whether gallbladder diseases contribute to hepatic disorders remains unknown. Methods: Here, we established an animal model of gallbladder dysfunction and assessed the role of a diseased gallbladder in cholestasis-induced hepatic fibrosis (CIHF). Results: Mice with smooth muscle-specific deletion of Mypt1, the gene encoding the main regulatory subunit of myosin light chain phosphatase (myosin phosphatase target subunit 1 [MYPT1]), had apparent dysfunction of gallbladder motility. This dysfunction was evidenced by abnormal contractile responses, namely, inhibited cholecystokinin 8-mediated contraction and nitric oxide–resistant relaxation. As a consequence, the gallbladder displayed impaired bile filling and biliary tract dilation comparable to the alterations in CIHF. Interestingly, the mutant animals also displayed CIHF features, including necrotic loci by the age of 1 month and subsequently exhibited progressive fibrosis and hyperplastic/dilated bile ducts. This pathological progression was similar to the phenotypes of the animal model with bile duct ligation and patients with CIHF. The characteristic biomarker of CIHF, serum alkaline phosphatase activity, was also elevated in the mice. Moreover, we observed that the myosin phosphatase target subunit 1 protein level was able to be regulated by several reagents, including lipopolysaccharide, exemplifying the risk factors for gallbladder dysfunction and hence CIHF. Conclusions: We propose that gallbladder dysfunction caused by myosin phosphatase target subunit 1 ablation is sufficient to induce CIHF in mice, resulting in impairment of the bile transport system.

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Section: Introductionmentioning

confidence: 67%

Gallbladder dysfunction caused by MYPT1 ablation triggers cholestasis-induced hepatic fibrosis in mice

Wang,

Jiang,

Zhou

et al. 2024

Hepatology Communications

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“…Parkman et al [12] demonstrated that after CBDL, an inhibitory NO pathway was also activated to help decrease gallbladder contractions in addition to the decreased cholinergic contractions. Recently, Gültekin et al [13] reported that the NOS inhibitor, NOARG, significantly increased the contractions induced by electrical field stimulation, and this increase in the contractions was reversed by L -arginine in guinea pig gallbladder strips in vitro conditions. CBDL causes gallbladder inflammation similar to acute acalculous cholecystitis [11] .…”

Section: Discussionmentioning

confidence: 99%

Effect of Nitric Oxide/Cyclic Guanosine Mono-phosphate Pathway on Gallbladder Relaxant Response in Bile Duct-Ligated Guinea Pigs

Aydın

Bağcıvan²,

Yıldırım³

et al. 2009

Eur Surg Res

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Background/Aims: Common bile duct ligation (CBDL) in the guinea pig is a well-defined model of acalculous cholecystitis. Nitric oxide (NO) mediates smooth muscle relaxation by stimulating the activity of soluble guanylate cyclase. The aim of this study was to determine whether the NO/cyclic guanosine monophosphate pathway plays a role in gallbladder relaxant response after CBDL. Methods: Relaxant response of gallbladder muscle strips from CBDL and sham-operated guinea pigs was studied in vitro. Animals were treated with saline, aminoguanidine or an aminoguanidine + L-arginine combination in vivo. Concentration-response curves of papaverine, diethylamine/NO, YC-1, sildenafil and amrinone were obtained and relaxations in each group were calculated as the percent of the contractions induced by carbachol (10^–6 M). Results: There was a significant decrease in the gallbladder muscle relaxant responses to these substances in CBDL and aminoguanidine groups compared with sham surgical controls. The decreased relaxant response was reversed by aminoguanidine + L-arginine but not by aminoguanidine alone. Conclusion: Decreased relaxant responses might be due to the reduced guanylate cyclase enzyme activity, but further studies are required.

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“…There could also be other mechanisms, of course. For example, nitric oxide also participates in the regulation of SO contractions 35 . The effect of acupuncture on these potential factors remains to be studied.…”

Section: Discussionmentioning

confidence: 99%

Bi-directional regulation of acupuncture on extrahepatic biliary system: An approach in guinea pigs

Zhao

Luo

et al. 2017

Sci Rep

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Clinically, acupuncture affects the motility of the extrahepatic biliary tract, but the underlining mechanisms are still unknown. We applied manual acupuncture (MA) and electrical acupuncture (EA) separately at acupoints Tianshu (ST25), Qimen (LR14), Yanglingquan (GB34), and Yidan (CO11) in forty guinea pigs (4 groups) with or without atropinization under anesthesia while Sphincter of Oddi (SO) myoelectric activities and gallbladder pressure were monitored. In both MA and EA groups, stimulation at ST25 or LR14 significantly increased the frequency and amplitude of SO myoelectrical activities and simultaneously decreased the gallbladder pressure as compared to the pre-MA and pre-EA (P < 0.05). On the contrary, stimulation at GB34 or CO11 significantly decreased SO myoelectricity and increased the gallbladder pressure (P < 0.05). Pretreatment with atropine could abolish the effect of stimulation at acupoints ST25, GB34 and LR14 (P > 0.05), although significant myoelectricity increases were still inducible with MA or EA stimulation at CO11 (P < 0.05). In summary, acupuncture has bi-directional effects to gallbladder pressure and SO function, which probably due to autonomic reflex and somatovisceral interactions.

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The Role of Nitric Oxide in the Electrical Field Stimulation-Induced Contractions of Sphincter of Oddi and Gallbladder Strips in Guinea Pigs

Cited by 8 publications

References 18 publications

Gallbladder dysfunction caused by MYPT1 ablation triggers cholestasis-induced hepatic fibrosis in mice

Gallbladder dysfunction caused by MYPT1 ablation triggers cholestasis-induced hepatic fibrosis in mice

Effect of Nitric Oxide/Cyclic Guanosine Mono-phosphate Pathway on Gallbladder Relaxant Response in Bile Duct-Ligated Guinea Pigs

Bi-directional regulation of acupuncture on extrahepatic biliary system: An approach in guinea pigs

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