Bronchial smooth muscle responses evoked by toluene diisocyanate are inhibited by ruthenium red and by indomethacin

Mapp, C. E.; Boniotti, Anna; Graf, Paul; Chitano, Pasquale; Fabbri, Leonardo M.; Nadel, Jay A.

doi:10.1016/0014-2999(91)90667-f

Cited by 24 publications

(14 citation statements)

References 20 publications

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“…For instance, Ueda et al [21] suggested that PGE1 enhanced, whereas indomethacin inhibited, the release of substance P from the trigeminal nerve terminals after electrical transmural stimulation of the isolated rabbit iris sphincter muscle. Moreover, Mapp et al [22] found that indomethacin in hibited the bronchoconstrictive effect of toluene diisocya nate, an effect that was at least partially mediated through the release of tachykinins [23]. Finally, we found that in domethacin prevented a phosphoramidon-dependent in crease in the contraction of guinea pig tracheas that were challenged with an antigen.…”

Section: Resultssupporting

confidence: 57%

Phosphoramidon Modulates Effects of the 5-Lipoxygenase Inhibition on Anaphylactic Contraction of the Guinea Pig Trachea

Tudorić

Coon²,

Bošnjak³

1994

Int Arch Allergy Immunol

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Our previous studies have shown that the inhibition of neutral endopeptidase, an enzyme which degrades tachykinins increases anaphylactic contraction of guinea pig tracheal smooth muscle. It was suggested that anaphylactic release of tachykinin-like substances is likely to be responsible for the observed increases in tracheal contractions. To obtain additional information on the mechanisms responsible for anaphylactic release of tachykinins in guinea pig trachea, we examined the effects of phosphoramidon, an inhibitor of neutral endopeptidase, on contractile response to antigen after preincubation with the selective 5-lipoxygenase inhibitor AA-861. AA-861 (5 μM) significantly reduced ovalbumin-induced contraction, although the effect was not constant. A marked spontaneous increase in contraction was observed. Phosphoramidon (10 μM) produced significant increase of this contraction (27% after 30 min, and 33% after 45 min). The addition of H₁-histamine receptor antagonist (diphenhydramine HCl,10 μM) produced additional inhibition of the initial phase of antigen-induced contraction, while its later phase, apart from a spontaneous increment in magnitude, remained similar. Phosphoramidon (10 μM) increased the contraction by 26% after 30 min, and by 34% after 45 min. Since the effects of histamine and 5-lipoxygenase pathway products were prevented, we hypothesize that cyclooxygenase pathway products are responsible for the phosphoramidon-dependent increase in antigen-induced contraction. In accordance with previously reported ineffectiveness of contractile prostaglandins, we suggest that the relaxant prostaglandins are most important in mediating the release of tachykinins during the immediate hypersensitivity reaction in guinea pig trachea.

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Section: Resultssupporting

confidence: 57%

Phosphoramidon Modulates Effects of the 5-Lipoxygenase Inhibition on Anaphylactic Contraction of the Guinea Pig Trachea

Tudorić

Coon²,

Bošnjak³

1994

Int Arch Allergy Immunol

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“…This observation is in congruence with previous studies showing that reactive airway irritants activate influx of calcium ions in a subset of capsaicin-sensitive neurons (52). Second, TRPA1 is blocked by ruthenium red, known to antagonize irritant-induced bronchoconstriction (5, 18, 84). Third, capsaicin pre-treatment renders C-fibers insensitive to both mustard oil and chemical airway irritants (20, 53).…”

Section: Trpa1 – More Than Just Spicementioning

confidence: 99%

Breathtaking TRP Channels: TRPA1 and TRPV1 in Airway Chemosensation and Reflex Control

2008

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New studies have revealed an essential role for TRPA1, a sensory neuronal TRP ion channel, in airway chemosensation and inflammation. TRPA1 is activated by chlorine, reactive oxygen species and noxious constituents of smoke and smog, initiating irritation and airway reflex responses. Together with TRPV1, the capsaicin receptor, TRPA1 may contribute to chemical hypersensitivity, chronic cough and airway inflammation in asthma, COPD and reactive airway dysfunction syndrome.

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“…It also inhibits neutral endopeptidase in experimental animals and in vitro preparations [110,111]. The activation of sensory nerves is likely to be indirect, through the release of prostanoids [112,113]. Mast cells play a role C.E.…”

Section: Neurogenic Inflammationmentioning

confidence: 99%

Mechanisms and pathology of occupational asthma

Mapp

Saetta²,

Maestrelli³

et al. 1994

Eur Respir J

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M Me ec ch ha an ni is sm ms s a an nd d p pa at th ho ol lo og gy y o of f o oc cc cu up pa at ti io on na al l a as st th hm ma a More than one mechanism may be operative in occupational asthma. Among the mechanisms proposed, immunological mechanisms and airway inflammation play an important role. There is evidence to confirm that T-lymphocyte activation and local accumulation in the bronchial wall of activated eosinophils occurs in asthma of diverse aetiology, i.e. immunoglobulin E (IgE)-mediated, occupational and intrinsic.Neurogenic pathways should be further investigated as a potential mechanism of modulation and amplification of airway inflammation in occupational asthma.

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Bronchial smooth muscle responses evoked by toluene diisocyanate are inhibited by ruthenium red and by indomethacin

Cited by 24 publications

References 20 publications

Phosphoramidon Modulates Effects of the 5-Lipoxygenase Inhibition on Anaphylactic Contraction of the Guinea Pig Trachea

Phosphoramidon Modulates Effects of the 5-Lipoxygenase Inhibition on Anaphylactic Contraction of the Guinea Pig Trachea

Breathtaking TRP Channels: TRPA1 and TRPV1 in Airway Chemosensation and Reflex Control

Mechanisms and pathology of occupational asthma

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