Production of arachidonic and linoleic acid metabolites by guinea pig tracheal epithelial cells

Oosthuizen, Mariëtha; Engels, Ferdi; Esch, Betty C.A.M. van; Henricks, Paul A.J.; Nijkamp, Frans P.

doi:10.1007/bf00914091

Cited by 16 publications

(6 citation statements)

References 29 publications

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“…ct-Adrenoreceptor agonists were shown to relax rat tracheal segments in an epithelium-dependent manner [1]. It has been suggested that ct-adrenoreceptors are located on the membrane of epitheliocytes and stimulate the production of relaxing factor through the cytosolic calcium mobilization [9,10]. It was shown that smooth muscle guanylate cyclase is involved in the regulation of epithelium-dependent relaxation revealed and is the target of NO and NO-producing compounds [2,8].…”

Section: Resultsmentioning

confidence: 99%

“…On the other hand, many researchers have noted a high concentration of eicosanoids in the airway wall epithelium and attributed epithelial relaxing effects to AA metabolites (prostaglandin E 2, prostacyclins) [9,11 ].…”

Section: Resultsmentioning

confidence: 99%

“…The mechanisms of this activity can be attributed to the ability of the respiratory epithelium to produce relaxing factors, whose nature and mechanisms of action remain unclear [6,7,9]. There is similarity beSiberian Medical University/, Research Institute of Mental Health, Siberian Division of the Russian Academy of Medical Sciences, Tomsk, Russia tween endothelial and epithelial relaxing factors and their possible cross-reactivity [1].…”

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confidence: 99%

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Role of guanylate cyclase and arachidonic acid metabolites in the regulation of epithelium-dependent relaxation of tracheal smooth muscles in rats

et al. 1999

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The effects of guanylate cyclase modulators and inhibitors of the arachidonic acid metabolism on epithelium-dependent smooth muscle reactions of rat tracheal segments were studied by a mechanographic technique. Application of phenylephrine to the tracheal segments precontracted by high-potassium Krebs' solution reduced their mechanical tension. This reaction was considerably less pronounced in the tracheal segments from which the epithelium had been removed. Phenylephrine-induced relaxation was suppressed by preincubation with methylene blue, but was not affected by preincubation with either indomethacin (a cyclooxygenase inhibitor) or nordihydroguaiaretic acid (a lipoxygenase inhibitor). These data suggest that the epithelium-dependent relaxation of the tracheal smooth muscle is mediated by guanylate cyclase activation, and arachidonic acid metabolites do not significantly contribute to this reaction.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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confidence: 99%

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Role of guanylate cyclase and arachidonic acid metabolites in the regulation of epithelium-dependent relaxation of tracheal smooth muscles in rats

et al. 1999

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“…It is known that fish oil, which contains n-3 fatty acids, possesses analgesic property and is used in various inflammatory disorders to alleviate pain [17,19,23,52]. Further, since SO is chiefly composed of linoleic acid, it may be possible that it is metabolized to 9- and 13-hydroxy-octadecadienoic acids (HODEs) [53,54] apart from AA and reduce the pain threshold in mice fed SO supplemented diet. Since formation of HODEs is inhibited by COX and LOX inhibitors [53,55], supplementing n-3 fatty acids may preferentially utilize these enzymes for the production of less potent PGE3 and LTB5.…”

Section: Discussionmentioning

confidence: 99%

Fish oil concentrate delays sensitivity to thermal nociception in mice

Veigas¹,

Williams²,

Halade³

et al. 2011

Pharmacological Research

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Fish oil has been used to alleviate pain associated with inflammatory conditions such as rheumatoid arthritis. The anti-inflammatory property of fish oil is attributed to the n-3 fatty acids docosahexaenoic acid and eicosapentaenoic acid. Contrarily, vegetable oils such as safflower oil are rich in n-6 fatty acids which are considered to be mediators of inflammation. This study investigates the effect of n-3 and n-6 fatty acids rich oils as dietary supplements on the thermally induced pain sensitivity in healthy mice. C57Bl/6J mice were fed diet containing regular fish oil, concentrated fish oil formulation (CFO) and safflower oil (SO) for 6 months. Pain sensitivity was measured by plantar test and was correlated to the expression of acid sensing ion channels (ASICs), transient receptor potential vanilloid 1 (TRPV1) and c-fos in dorsal root ganglion cells. Significant delay in sensitivity to thermal nociception was observed in mice fed CFO compared to mice fed SO (p<0.05). A significant diminution in expression of ion channels such as ASIC1a (64%), ASIC13 (37%) and TRPV1 (56%) coupled with reduced expression of c-fos, a marker of neuronal activation, was observed in the dorsal root ganglion cells of mice fed CFO compared to that fed SO. In conclusion, we describe here the potential of fish oil supplement in reducing sensitivity to thermal nociception in normal mice.

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“…This labile intermediate is further reduced to its 13-hydroxy derivative, 13-hydroxylinoleic acid (13-HODE). 13-HODE is present in and can be produced by several cell types including endothelial cells (Buchanan et al, 1985), neutrophils (Sobermann et al, 1985), epithelial cells (Oosthuizen et al, 1990) and macrophages (Engels et al, 1986). However, the biological activity of 13-HODE has been mainly investigated in vitro.…”

Section: Introductionmentioning

confidence: 99%

Hypotensive effect of 13‐hydroxylinoleic acid in the rat: mediation via the release of a CGRP‐like mediator from capsaicin‐sensitive nerves

Heuven-Nolsen

Muis

Engels

et al. 1995

British J Pharmacology

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1. The effect of 13-hydroxylinoleic acid (13-HODE) on changes in blood pressure in the rat was measured. 2. 13-HODE (0.1 - 100 micrograms kg-1) had no direct effect on blood pressure in the rat and had no effect on histamine (0.1 - 1000 micrograms kg-1)-induced changes in blood pressure. In contrast, it was found that 13-HODE itself induced a decrease in diastolic arterial blood pressure when it was injected intravenously after either a single dose of histamine (10, 100 or 1000 micrograms kg-1) or after a dose-response curve of histamine (0.1 - 1000 micrograms kg-1). 3. This hypotensive effect of 13-HODE was not observed after administration of the endothelium-dependent vasodilator, acetylcholine (0.1 - 10 micrograms kg-1), the endothelium-independent vasodilator, sodium nitroprusside (0.1 - 100 micrograms kg-1) or the inflammatory mediator, leukotriene B4 (0.1 - 300 micrograms kg-1). However, prior injection of bradykinin (0.1 - 100 micrograms kg-1) allowed a dose-dependent hypotensive effect of 13-HODE to be revealed. 4. The hypotensive effect of 13-HODE after histamine and bradykinin could be inhibited by neonatal capsaicin treatment of the rats (50 mg kg-1, s.c. on day 1 and 2 after birth). 5. Ruthenium red (120 micrograms kg-1 min-1), an inhibitor of excitatory effects on sensory nerves, and the CGRP antagonist, CGRP8-37 (1-3 micrograms kg-1 min-1) also inhibited the hypotensive effect of 13-HODE. 6. It is concluded that the hypotensive effect of 13-HODE in the rat after histamine and bradykinin is due to the release of a CGRP-like substance from sensory nerves. These results highlight the possibility that endogenous 13-HODE could be involved in the neurogenic regulation of blood pressure.

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Production of arachidonic and linoleic acid metabolites by guinea pig tracheal epithelial cells

Cited by 16 publications

References 29 publications

Role of guanylate cyclase and arachidonic acid metabolites in the regulation of epithelium-dependent relaxation of tracheal smooth muscles in rats

Role of guanylate cyclase and arachidonic acid metabolites in the regulation of epithelium-dependent relaxation of tracheal smooth muscles in rats

Fish oil concentrate delays sensitivity to thermal nociception in mice

Hypotensive effect of 13‐hydroxylinoleic acid in the rat: mediation via the release of a CGRP‐like mediator from capsaicin‐sensitive nerves

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