Monochloramine induces contraction of guinea pig gallbladder via two different pathways

Moummi, Chafiq; Gullikson, Gary W.; Gaginella, Timothy S.

doi:10.1152/ajpgi.1991.260.6.g881

Cited by 10 publications

(25 citation statements)

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“…ROS have been shown to disrupt intestinal motility, causing an initial contraction followed by a slow relaxation as well as blocking the contraction induced by methacholine (37). They also inhibit the gallbladder muscle contraction induced by CCK-8, ACh, and KCl in muscle strips (10,23,25).…”

Section: Discussionmentioning

confidence: 96%

“…These abnormalities are characterized by 1) inhibition of the contraction induced by agonists that are membrane dependent (CCK, ACh, KCl) without affecting the actions of GTP␥S, DAG, and IP 3 that circumvent membrane receptors; 2) depletion of membrane phospholipids, increased cholesterol-to-phospholipid ratio, and lipid peroxidation, which could decrease the membrane fluidity; 3) lower 125 I-labeled CCK-8 binding capacity; and 4) increase in PGE 2 levels and SOD and catalase activities. Therefore, the muscle abnormalities observed in acute cholecystitis may be due to the actions of ROS on muscle cells (23). The preservation of the PGE 2 -induced contraction suggests that the increased production of this eicosanoid may protect its membrane receptors (13).…”

Section: Discussionmentioning

confidence: 99%

“…Acute cholecystitis is characterized by an inflammatory process that involves the gallbladder wall with polymorphonuclear cells (23). ROS play a major role in mediating cell injury during inflammatory processes.…”

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confidence: 99%

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Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Xiao

Andrada²,

Biancani

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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The level of lipid peroxidation as well as the PGE2 content was significantly increased after H2O2 pretreatment. Unlike superoxide dismutase, the free radical scavenger catalase prevented the H2O2 induced contraction, and its inhibition of the CCK-8 induced contraction. It is concluded that ROS cause damage to the plasma membrane of the gallbladder muscle and contraction through the generation of PGE2 induced by cPLA2-cyclooxygenase and probably mediated by the PKC-MAPK pathway. lipid peroxidation; prostaglandin E2 content; smooth muscle REACTIVE OXYGEN SPECIES (ROS) such as superoxide radical anion, hypochlorous acid, and hydrogen peroxide (H 2 O 2 ) are by-products of oxidative metabolism, in which energy activation and electron reduction are involved. Inflammatory processes enhance their production, which could affect cell functions (20). The mechanisms whereby ROS act at the cellular level are not fully understood. Their pathogenic role on cell membranes and signal-transduction pathways may explain the early events that are associated with cell dysfunction caused by inflammation. Therefore, the understanding of these mechanisms is important for developing therapeutic strategies at cellular sites of dysfunction.Acute cholecystitis is characterized by an inflammatory process that involves the gallbladder wall with polymorphonuclear cells (23). ROS play a major role in mediating cell injury during inflammatory processes. Disorders of gallbladder motility caused or aggravated by inflammatory processes may be due to the actions of ROS. They may also contribute to the inhibition of agonist-induced contraction (25, 37). The actions of ROS are mediated in part by cyclooxygenase by-products that are important participants in the inflammatory process (16). The contraction of tracheal and ileal muscle strips induced by ROS in vitro appear to be mediated by prostaglandins (24,29).Prostaglandins have varied effects on gastrointestinal motility (5,12,17,32). Muscle strips from various segments of guinea pig stomach exhibited different responses to PGE 1 , PGE 2 , and PGF 2␣ (22). In rat stomach, PGE 2 caused a contraction in the longitudinal preparation but had no effect on the circular muscle (35). PGE 1 , PGE 2 , and PGF 2␣ potentiated the contractile responses of guinea pig gallbladder to transmural stimulation and ACh (28). Prostaglandins may also be involved in muscle cytoprotection since PGE 2 and other prostaglandins appear to participate in the pathway responsible for increased formation of scavengers of free radicals (2). These studies therefore were aimed at examining the effects of ROS on gallbladder muscle function utilizing H 2 O 2 on enzymatic digested single muscle cells from normal guinea pig gallbladders. MATERIALS AND METHODSAnimals. Adult male guinea pigs were purchased from Elm Hill Breeding Laboratory (Chelmsford, MA). The Animal Welfare Committee of Rhode Island Hospital approved their use. Animals were housed in thermoregulated rooms and had free access to food and water. After an overnight fast, th...

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Xiao

Andrada²,

Biancani

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…After 1 h of equilibrium at a resting tension of 1 g, which was reported to be optimal for the measurement of changes in the tension of gallbladder strips from guinea pigs [7], the strips were contracted with 60 mmol/l KCl. After washing out the bath solution, the KCl contraction protocol was repeated once more.…”

Section: Measurement Of the Isometric Tensionmentioning

confidence: 99%

Diminished Inibitory Action of Ethanol on the Contraction of Gallbladder Isolated from Chronically Ethanol-Fed Guinea Pigs

Masui

Wakabayashi²,

Siogawa³

et al. 2002

Pharmacology

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Ethanol is known to decrease the gallbladder contractility. The purpose of this study was to clarify the mechanism of tolerance to the inhibitory action of ethanol on the gallbladder contractility. Male guinea pigs were fed ethanol (3%) or calorie-matched sucrose in the drinking water for 4 weeks. Then, the gallbladder was isolated, and its isometric tension was measured. The contractile responses to KCl, BAY K8644, histamine, and phorbol 12,13-dibutyrate in the normal medium were not different between the gallbladder strips from ethanol-fed and control guinea pigs. Ethanol at 25 mmol/l in vitro did not affect the contractile responses to KCl and BAY K8644 in the gallbladder strips from both ethanol-fed and control guinea pigs. On the other hand, ethanol at 25 mmol/l in vitro significantly inhibited the contractile responses to histamine and phorbol 12,13-dibutyrate in the gallbladder strips from the control guinea pigs, but it did not affect the contractile response to histamine and significantly augmented that to phorbol 12,13-dibutyrate in the strips from the ethanol-fed guinea pigs. Diphenhydramine, a selective H₁ receptor antagonist, abolished the histamine contraction in gallbladder strips from both control and ethanol-fed guinea pigs, while cimetidine, a selective H₂ receptor antagonist, did not affect histamine contraction, implying that histamine-induced contraction of guinea pig gallbladders is mediated only by H₁ receptors. Verapamil (1 µmol/l) completely inhibited the phorbol 12,13-dibutyrate-induced contraction of the strips from both ethanol-fed and control guinea pigs. The histamine-induced contraction was partly inhibited in the absence of Ca²⁺ in the medium. In the gallbladder strips from both ethanol-fed and control guinea pigs, ethanol at 25 mmol/ in vitro did not affect the histamine-induced contraction in the absence of extracellular Ca²⁺. Tolerance to the inhibitory action of ethanol developed selectively on contractile responses to histamine and phorbol 12,13-dibutyrate. Chronic ethanol administration produces tolerance to in vitro gallbladder contractility mediated by the Ca²⁺ entry through L-type Ca²⁺ channels linked with protein kinase C activation.

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“…Lipid peroxidation results in the generation of isoprostanes, platelet-activating factor (PAF)-like lipids (10), and oxidized byproducts. Isoprostanes do not appear to be plausible candidates of stimulating the pathways that mediate the contraction and cytoprotective responses, because they tend to behave like prostaglandin receptor antagonists; particularly against PGF 2␣ (12)(13)(14)16). Other oxidation products of phosphatidylcholine bind and activate PAF receptors (19).…”

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confidence: 99%

PAF-like lipids- and PAF-induced gallbladder muscle contraction is mediated by different pathways in guinea pigs

Guarino

Zuo

Biancani

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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H2O2 stimulates gallbladder muscle contraction and scavengers of free radicals through the generation of PGE2. Oxidative stress causes lipid peroxidation and generation of platelet-activating factor (PAF) or PAF-like lipids. The present studies therefore were aimed at determining whether either one induced by H2O2 mediates the increased generation of PGE2. Dissociated muscle cells of guinea pig gallbladder were obtained by enzymatic digestion. Both PAF-like lipids and PAF-induced muscle contraction was blocked by the PAF receptor antagonist CV-3988. This antagonist also blocked the increased PGE2 production caused by PAF-like lipids or PAF. Actions of PAF-like lipids were completely inhibited by indomethacin, but those of PAF were only partially reduced by indomethacin or by nordihydroguaiaretic acid and completely blocked by their combination. PAF-like lipids-induced contraction was inhibited by AACOCF3 (cystolic phospholipase A2 inhibitor), whereas the actions of PAF were blocked by MJ33 (secretory phospholipase A2 inhibitor). Receptor protection studies showed that pretreatment with PAF-like lipids before N-ethylmaleimide protected the contraction induced by a second dose of PAF-like lipids or PGE2 but not by PAF. In contrast, pretreatment with PAF protected the actions of PAF and PGE2 but not that of PAF-like lipids. Both PAF-like lipids and PAF-induced contractions were inhibited by anti-Gαq/11 antibody and by inhibitors of MAPK and PKC. In conclusion, PAF-like lipids seem to activate a pathway different from that of PAF probably by stimulating a different PAF receptor subtype.

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Monochloramine induces contraction of guinea pig gallbladder via two different pathways

Cited by 10 publications

References 0 publications

Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Diminished Inibitory Action of Ethanol on the Contraction of Gallbladder Isolated from Chronically Ethanol-Fed Guinea Pigs

PAF-like lipids- and PAF-induced gallbladder muscle contraction is mediated by different pathways in guinea pigs

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Monochloramine induces contraction of guinea pig gallbladder via two different pathways

Cited by 10 publications

References 0 publications

Reactive oxygen species (H2O2): effects on the gallbladder muscle of guinea pigs

Reactive oxygen species (H2O2): effects on the gallbladder muscle of guinea pigs

Diminished Inibitory Action of Ethanol on the Contraction of Gallbladder Isolated from Chronically Ethanol-Fed Guinea Pigs

PAF-like lipids- and PAF-induced gallbladder muscle contraction is mediated by different pathways in guinea pigs

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Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs