The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs <i>in vivo</i>

Ichinose, Masakazu; Barnes, Peter J.

doi:10.1111/j.1476-5381.1990.tb12092.x

Cited by 37 publications

(17 citation statements)

References 20 publications

(15 reference statements)

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“…This contrasts with observations made in anesthetized guinea pigs where intravenous (Ichinose and Barnes, 1990a;Wirth et al, 1993;Tramontana et al, 2001), intratracheal (Ichinose and Barnes, 1990b), or inhaled (Sakamoto et al, 1994) bradykinin exerted bronchoconstriction. The lack of effect of inhaled bradykinin in conscious guinea pigs seems to be caused by the rapid breakdown of bradykinin because there was a significant bronchoconstriction after treatment with captopril, an ACE inhibitor.…”

Section: Discussioncontrasting

confidence: 52%

“…NEP is expressed in the respiratory epithelium (Baraniuk et al, 1995), so inhalation exposure would enable phosphoramidon to have an instant effect, whereas after intraperitoneal injection the drug may not be reaching the lung in a concentration sufficient to inhibit NEP. Captopril and phosphoramidon were shown to potentiate the bronchoconstriction by airway-instilled bradykinin in anesthetized guinea pigs (Ichinose and Barnes, 1990b) and intravenous (Chodimella et al, 1991). The kininase I inhibitor DL-2-mercaptomethyl-3-guanidinoethylthiopropionic acid (MGTA) failed to alter the bronchoconstriction in both of these studies.…”

Section: Discussionmentioning

confidence: 99%

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Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Broadley

Blair²,

Kidd³

et al. 2010

J Pharmacol Exp Ther

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Inhaled bradykinin causes bronchoconstriction in asthmatic subjects but not nonasthmatics. To date, animal studies with inhaled bradykinin have been performed only in anesthetized guinea pigs and rats, where it causes bronchoconstriction through sensory nerve pathways. In the present study, airway function was recorded in conscious guinea pigs by whole-body plethysmography. Inhaled bradykinin (1 mM, 20 s) caused bronchoconstriction and influx of inflammatory cells to the lungs, but only when the enzymatic breakdown of bradykinin by angiotensin-converting enzyme and neutral endopeptidase was inhibited by captopril (1 mg/kg i.p.) and phosphoramidon (10 mM, 20-min inhalation), respectively. The bronchoconstriction and cell influx were antagonized by the B 2 kinin receptor antagonist 4-(S)-amino-5-(4-{4-[2, 4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido]-tetrahydro-2H-4-pyranylcarbonyl}piperazino)-5-oxopentyl](trimethyl)ammonium chloride hydrochloride (MEN16132) when given by inhalation (1 and 10 M, 20 min) and are therefore mediated via B 2 kinin receptors. However, neither intraperitioneal MEN16132 nor the peptide B 2 antagonist icatibant, by inhalation, antagonized these bradykinin responses. Sensitization of guinea pigs with ovalbumin was not sufficient to induce airway hyperreactivity (AHR) to the bronchoconstriction by inhaled bradykinin. However, ovalbumin challenge of sensitized guinea pigs caused AHR to bradykinin and histamine. Infection of guinea pigs by nasal instillation of parainfluenza-3 virus produced AHR to inhaled histamine and lung influx of inflammatory cells. These responses were attenuated by the bradykinin B 2 receptor antagonist MEN16132 and H-(4-chloro)DPhe-2Ј(1-naphthylalanine)-(3-aminopropyl)guanidine (VA999024), an inhibitor of tissue kallikrein, the enzyme responsible for lung synthesis of bradykinin. These results suggest that bradykinin is involved in virus-induced inflammatory cell influx and AHR.

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Section: Discussioncontrasting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Broadley

Blair²,

Kidd³

et al. 2010

J Pharmacol Exp Ther

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“…NK receptor-dependent axonal reflexes may also contribute to the airway responses evoked by bradykinin in guinea pigs (Nakajima et al, 1994;Joad et al, 1997). However, we observed that drugs that prevent bradykinin-induced bronchospasm did not prevent bradykinin-induced coughing, while drugs that would be expected to enhance bradykinin-induced bronchospasm (e.g., captopril, L-NNA, and thiorphan) (Ichinose and Barnes, 1990;Ricciardolo et al, 1994b) did not, on their own, enhance bradykinin-evoked coughing.…”

Section: Discussioncontrasting

confidence: 50%

Pharmacology of Bradykinin-Evoked Coughing in Guinea Pigs

Hewitt

Adams

Mazzone

et al. 2016

Journal of Pharmacology and Experimental Therapeutics

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Bradykinin has been implicated as a mediator of the acute pathophysiological and inflammatory consequences of respiratory tract infections and in exacerbations of chronic diseases such as asthma. Bradykinin may also be a trigger for the coughing associated with these and other conditions. We have thus set out to evaluate the pharmacology of bradykinin-evoked coughing in guinea pigs. When inhaled, bradykinin induced paroxysmal coughing that was abolished by the bradykinin B 2 receptor antagonist HOE 140. These cough responses rapidly desensitized, consistent with reports of B 2 receptor desensitization. Bradykinin-evoked cough was potentiated by inhibition of both neutral endopeptidase and angiotensin-converting enzyme (with thiorphan and captopril, respectively), but was largely unaffected by muscarinic or thromboxane receptor blockade (atropine and ICI 192605), cyclooxygenase, or nitric oxide synthase inhibition (meclofenamic acid and N G

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“…In experiments with bradykinin, all animals were pretreated with captopril (5mg kg 1) 15min before the beginning of the experiment to block bradykinin metabolism (Ichinose & Barnes, 1990a) and potentiate its effects.…”

Section: Measurement Ofairway Resistancementioning

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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The effect of peptidase inhibitors on bradykinin‐induced bronchoconstriction in guinea‐pigs in vivo

Cited by 37 publications

References 20 publications

Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Pharmacology of Bradykinin-Evoked Coughing in Guinea Pigs

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

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