Effects of tachykinins on mucus secretion in human bronchi in vitro

Rogers, Duncan F.; Aursudkij, B; Barnes, Peter J.

doi:10.1016/0014-2999(89)90322-1

Cited by 118 publications

(42 citation statements)

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“…In human bronchial smooth muscle, natural tachykinins (TKs) (substance P, neurokinin A, neurokinin B) act as potent inducers of mucus secretion (Rogers et al, 1989) and smooth muscle contraction (Advenier et al, 1987;Honda et al, 1991). Previous studies have clearly identified the NK2 receptor as responsible for the TKinduced bronchoconstriction (Naline et al, 1989;Dion et al, 1990a;Rhoden & Barnes, 1990).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the tachykinin NK₂ receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Astolfi

Treggiari

Giachetti

et al. 1994

British J Pharmacology

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4 In the presence of amastatin the pseudopeptide MDL28,564 behaved as a partial agonist. 5 We conclude that the NK2 receptor subtype present in the human bronchus has properties similar to those described for the circular muscle of the human colon and thus may be classified as a 'NK2A' subtype. We show that the apparent potency of peptides, bearing N-terminal acidic residues, is influenced by an amastatin-sensitive peptidase, possibly aminopeptidase A.

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Section: Introductionmentioning

confidence: 99%

Characterization of the tachykinin NK₂ receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Astolfi

Treggiari

Giachetti

et al. 1994

British J Pharmacology

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“…Activation of tachykinin receptors in the airways could lead to bronchoconstriction, hyperreactivity and inappropriate secretion of mucus (see for example Saria et al, 1985;Barnes, 1986;Martling et al, 1987;Crimi & Mistretta, 1989;Joos, 1989;Rogers et al, 1989). Elucidation of the precise role (if any) of tachykinins in asthma is likely to be facilitated by an understanding of the tachykinin receptors present in airways.…”

Section: Introductionmentioning

confidence: 99%

Receptors mediating tachykinin‐induced contractile responses in guinea‐pig trachea

Ireland

Bailey

Cook

et al. 1991

British J Pharmacology

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1 The classification of tachykinin receptors in the guinea-pig trachea has been investigated. This 5 For L-659,877 and R396, comparison was made between activity in guinea-pig trachea and in preparations known to contain tachykinin receptors predominantly of the NK2 type. In the rabbit trachea, both L-659,877 and R396 had effects similar to those in guinea-pig trachea. In contrast, in the rat colon muscularis mucosae, both L-659,877 and R396 appeared to behave competitively with pKB values against GR64349 of 7.83 and 6.90 respectively. 6 It is concluded that in guinea-pig trachea, contractile responses can be induced by activation of both NK1 and NK2 receptors. The present data are discussed with reference to the proposed existence of subtypes of the NK2 receptor.

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“…Another system implicated in airway inflammatory responses, which could be triggered by loss or alteration of the epithelial surface, is neurogenic inflammation. Stimulation of sensory nerves in airway epithelium releases tachykinins including substance P and neurokinins A and B [23][24][25][26][27]. Tachykinins specifically cause chemotaxis and adhesion of neutrophils in the airway circulation [28,29], stimulate the release of inflammatory cytokines and cause degranulation of eosinophils [30,31].…”

Section: The Cellular Inflammatory Infiltrate In the Airwaysmentioning

confidence: 99%

Disease of the airways in chronic obstructive pulmonary disease

Piqueras

Cosio²

2001

Eur Respir J

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The pathological hallmarks of chronic obstructive pulmonary disease (COPD) are inflammation of the small airways (bronchiolitis) and destruction of lung parenchyma (emphysema). The functional consequence of these abnormalities is airflow limitation.Airway abnormalities and emphysema interact in a complex fashion in the development of airflow limitation in COPD. In an attempt to improve understanding of the role of the airways in COPD, the morphological counterparts of airflow limitation, the cellular inflammatory infiltrate in the airways and the relationship between emphysema type and airway abnormalities are reviewed.Significant correlation between airway remodelling and functional measurements are found in earlier stages of COPD. In advanced COPD, airflow limitation is reflected by airway narrowing, airway deformity and extent of emphysema. The cellular inflammatory infiltrate is mainly composed of neutrophils in early stages of COPD. However, the presence of CD8z T-cells seems to differentiate smokers with COPD from smokers that would not develop the disease. The inflammatory changes and remodelling found in the airways and their contribution to airflow obstruction might be modulated by the type of emphysema smokers develop, with centrilobular emphysema showing more severe inflammatory changes and narrower airways than panlobular emphysema.In conclusion, the degree of airway involvement in chronic obstructive pulmonary disease can vary greatly for the same degree of airflow obstruction, depending on the type of emphysema smokers develop. If the underlying lung abnormalities in chronic obstructive pulmonary disease vary, as the evidence suggests, the study of cigaretteinduced lung disease as a single entity will further delay understanding of chronic obstructive pulmonary disease. The pathological hallmarks of chronic obstructive pulmonary disease (COPD) are inflammation of the small airways (bronchiolitis) and destruction of lung parenchyma (emphysema). The functional consequence of these abnormalities is airflow limitation.Bronchiolitis contributes to airflow limitation by narrowing and obliterating the airway lumen and by actively constricting the airway. Emphysema, by reducing the elastic recoil of the lung through parenchymal destruction and increase in alveolar size, as well as reducing the elastic load applied to the airways through destruction of alveolar attachments, also contributes to the airflow limitation characteristic of smokers. Although there is increasing evidence that the large airways are inflamed in patients with COPD, this is not believed to contribute directly to the airflow limitation in these patients.It has become apparent that airway abnormalities and emphysema interact in a complex fashion, rather than simply additively in the development of airflow limitation and COPD. The type of emphysema that smokers develop seems to determine, to a great extent, the quantity and possibly type of inflammation and airway remodelling found, suggesting that different pathogenetic mechani...

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Effects of tachykinins on mucus secretion in human bronchi in vitro

Cited by 118 publications

References 9 publications

Characterization of the tachykinin NK₂ receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Characterization of the tachykinin NK₂ receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Receptors mediating tachykinin‐induced contractile responses in guinea‐pig trachea

Disease of the airways in chronic obstructive pulmonary disease

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Effects of tachykinins on mucus secretion in human bronchi in vitro

Cited by 118 publications

References 9 publications

Characterization of the tachykinin NK2 receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Characterization of the tachykinin NK2 receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Receptors mediating tachykinin‐induced contractile responses in guinea‐pig trachea

Disease of the airways in chronic obstructive pulmonary disease

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Product

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Characterization of the tachykinin NK₂ receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways

Characterization of the tachykinin NK₂ receptor in the human bronchus: influence of amastatin‐sensitive metabolic pathways