Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Rogers, Duncan F.; Dijk, Sas; Barnes, Peter J.

doi:10.1111/j.1476-5381.1990.tb14150.x

Cited by 52 publications

(29 citation statements)

References 35 publications

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“…For example, Y-24180 exhibited 33% inhibition in the trachea. This finding is in agreement with that in a previous paper (25) in which the apparent bradykinin-induced leakage in guinea pigs was found to be also partially mediated by PAF, prostaglandins and other substances. All of these results demonstrate that Y-24180 acts as a selective PAF-receptor antagonist on airway microvascular leakage and that PAF is not involved in the airway inflammatory responses mediated by LTD,, and those by histamine.…”

Section: Antigen-induced Airway Microvascular Leakagesupporting

confidence: 83%

Effect of Y-24180, a Platelet-Activating Factor-Receptor Antagonist, on the Antigen-Induced Airway Microvascular Leakage in Guinea Pigs

Iwahisa¹,

Yamaguchi²,

Kagoshima³

et al. 1996

Japanese Journal of Pharmacology

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ABSTRACT-The inhibitory effect of Y-24180 ((±)-4-(2-chlorophenyl)-2-[2-(4-isobutylphenyl)ethyl]-6,9-dimethyl-6H-thieno [3,2-on platelet-activating factor (PAF)-or antigen-induced airway microvascular leakage was studied in guinea pigs by oral administration. The tissue content of extravasated Evans blue dye was used as an index of plasma exudation in the trachea, main bronchi, central intrapulmonary airways and peripheral intrapulmonary airways. In all of these tissues, Y-24180 potently inhibited the leakage induced by PAF. The ED50 value of Y-24180 determined in each of the tissues was approximately 0.02 mg/kg, demonstrating that the inhibitory potency of Y-24180 is 4-6 times that of WEB 2086, another PAF antagonist. Even at a dose of 10 mg/kg, however, Y-24180 showed no inhibitory effect on the leakage induced by leukotriene (LT) D4, histamine or bradykinin. In the antigeninduced model of guinea pigs sensitized with aerosolized ovalbumin, Y-24180 (0.1-10 mg/kg) and WEB 2086 (1-100 mg/kg) potently inhibited the microvascular leakage in all of the examined airway tissues except for the trachea. At 1-100 mg/kg, however, both ONO-1078, an LT-receptor antagonist, and OKY-046, a thromboxane A2 synthetase inhibitor, prevented partially but not significantly the antigen-induced leakage. These results provide evidence that endogenous PAF partially mediates the antigen-induced airway microvascular leakage in guinea pigs.

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Section: Antigen-induced Airway Microvascular Leakagesupporting

confidence: 83%

Effect of Y-24180, a Platelet-Activating Factor-Receptor Antagonist, on the Antigen-Induced Airway Microvascular Leakage in Guinea Pigs

Iwahisa¹,

Yamaguchi²,

Kagoshima³

et al. 1996

Japanese Journal of Pharmacology

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“…Besides its bronchocontractile properties, BK is a well known vasoactive peptide, and has been shown to increase vascular permeability in guinea-pig airways (Saria et al, 1983;Rogers et al, 1990). Moreover, an autoradiographic study of human lung has revealed a high density of BK binding sites on bronchial and pulmonary blood vessels (Mak & Barnes, 1991).…”

Section: Methodsmentioning

confidence: 99%

Bradykinin binding sites in healthy and carcinomatous human lung

Lach

Dumont²,

Gies

1994

British J Pharmacology

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“…Both intravenous and inhaled bradykinin cause bronchoconstriction in asthmatic, but not in normal subjects (Simonsson et al, 1973;Newball et al, 1975;Fuller et al, 1987;). Bradykinin causes not only bronchoconstriction but also stimulation of sensory nerves (Kaufman et al, 1980;Dixon & Barnes, 1989), increase of mucus secretion (Davies et al, 1982) and airway microvascular leakage with oedema formation (Saria et al, 1983;Rogers et al, 1990), which may be relevant to asthma (Persson, 1987;Chung et al, 1990). Concerning the upper 1 Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Formoterol and salbutamol inhibit bradykinin‐ and histamine‐induced airway microvascular leakage in guinea‐pig

Advenier¹,

Qian²,

Koune³

et al. 1992

British J Pharmacology

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1 The effects of the #2-adrenoceptor agonists, salbutamol and formoterol, on the increase of microvascular permeability induced by histamine or bradykinin in guinea-pig airways have been studied in vivo. Extravasation of intravenously injected Evans blue dye was used as an index of permeability. The effects of salbutamol and formoterol on the increase in pulmonary airway resistance induced by histamine or bradykinin have also been studied. 2 The increase in pulmonary airway resistance induced by histamine or bradykinin was totally inhibited by salbutamol and formoterol. The ED50 of the two mediators were 0.59 + 0.21 (n = 5) and 0.20 + 0.14 (n = 5) pg kg'-respectively for salbutamol, and 0.13 + 0.12 (n = 6) and 0.02 + 0.01 (n = 6) pg kgrespectively for formoterol.3 Salbutamol (10 and 30pgkg-1) and formoterol (1 and lOpgkg-1) inhibited the increase of microvascular permeability induced by histamine (30pgkg-') in the guinea-pig airways. The inhibitory effect was predominant in the trachea and the main bronchi, with a maximum inhibition of 20 to 50%. The two drugs had little or no inhibitory effect on the other structures studied, viz. nasal mucosa, larynx, proximal and distal intrapulmonary airways.4 Salbutamol and formoterol (1 and 10pgkg-1) abolished the increase in microvascular permeability induced by bradykinin (0.3 Mg kg'-). This inhibitory effect of two f-adrenoceptor stimulants was predominant in the trachea and the nasal mucosa where it was observed with 1 pg kg-1 of the f-adrenoceptor agonists. In the main bronchi, and in the proximal and distal intrapulmonary airways, the effects of bradykinin were abolished by 10 pg kg -of formoterol and salbutamol. 5 The effects of bradykinin, but not those of histamine, were significantly reduced (nasal mucosa, main bronchi and distal intrapulmonary airways) or abolished (trachea, proximal intrapulmonary airways) by morphine 10mgkg-1, i.v. These results suggest that an indirect effect, through non-adrenergic noncholinergic (NANC) nerves is involved in the action of bradykinin on the microvascular permeability. 6 In conclusion, intravenously injected f-adrenoceptor stimulants can inhibit, partially or totally, the increase of airways microvascular permeability induced by intravenous histamine or bradykinin. However, these effects require doses that are higher than those that inhibit the increase in pulmonary airway resistance induced by these mediators. As suggested by the results obtained with morphine, the higher efficacy of fi2-adrenoceptor agonists versus bradykinin may occur through activation of presynaptic receptors of the non-adrenergic non-cholinergic (NANC) nerves preventing release of inflammatory neuropeptides such as substance P and neurokinin A.

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Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Cited by 52 publications

References 35 publications

Effect of Y-24180, a Platelet-Activating Factor-Receptor Antagonist, on the Antigen-Induced Airway Microvascular Leakage in Guinea Pigs

Effect of Y-24180, a Platelet-Activating Factor-Receptor Antagonist, on the Antigen-Induced Airway Microvascular Leakage in Guinea Pigs

Bradykinin binding sites in healthy and carcinomatous human lung

Formoterol and salbutamol inhibit bradykinin‐ and histamine‐induced airway microvascular leakage in guinea‐pig

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