‘Sensory‐efferent’ neural control of mucus secretion: characterization using tachykinin receptor antagonists in ferret trachea <i>in vitro</i>

Ramnarine, S.I.; Hirayama, Yoshitaka; Barnes, Peter J.; Rogers, Duncan F.

doi:10.1111/j.1476-5381.1994.tb17122.x

Cited by 44 publications

(27 citation statements)

References 38 publications

(59 reference statements)

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“…This is consistent with the relative scarceness ofSP immunoreactive nerves in human airways compared with the airways ofsmall laboratory animals [13][14][15][16]. Thus, as an example, although acute administration of capsaicin to human airway tissue in vitro induces contraction [17] and mucus secretion [18], compared with the equivalent system in animal airways, much higher concentrations ofcapsaicin are required and the response is markedly less [19,20]. In animal airways, electrical stimulation of tissue in the presence of adrenergic and cholinergic blockade reveals non-adrenergic, non-cholinergic (NANC) neural mechanisms, of which excitatory and inhibitory pathways can be demonstrated [7,10].…”

Section: Acutestudiessupporting

confidence: 78%

Neurogenic inflammation in lung disease: Burnt out?

Rogers

1997

Inflammopharmacol

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Neurogenic inflammation results from activation of sensory nerves which, acting in an 'efferent' manner, release sensory neuropeptides to induce a wide variety of physiological and immunological responses. This process is easy to demonstrate experimentally in the airways of small laboratory animal species but in human airways is equivocal and, at best, minor compared with cholinergic neural control. Nevertheless, sensory neuropeptides (calcitonin gene-related peptide and the tachykinins, substance P and neurokinin A) induce airway responses in both laboratory animals and humans which suggest a potential for sensory-efferent control of human airways. In addition, there is indirect evidence for an increased 'expression' of sensory nerves and tachykinin receptors in asthma and bronchitis, which indicates that neurogenic inflammation contributes to pathophysiology of these airway conditions. In contrast, clinical trials using different classes of drugs to inhibit sensory nerve responses have failed to resolve whether neurogenic inflammation is involved in asthma, although there are concerns about the relevance of some of these studies. In contrast to their involvement in airway neurogenic inflammation, sensory nerves may be important in initiating protective reflexes, including coughing and sneezing, acting via their afferent pathways. Thus, although flickering, the concept of neurogenic inflammation in lung disease is not yet burnt out. However, it needs the rekindling of interest which re-evaluation as a protective process may bring, together with data from more appropriate clinical studies in asthma and chronic bronchitis.

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Section: Acutestudiessupporting

confidence: 78%

Neurogenic inflammation in lung disease: Burnt out?

Rogers

1997

Inflammopharmacol

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“…Further evidence for this hypothesis is provided by their work demonstrating increased expression of substance P and its receptor in asthmatics, which was correlated with the mucus content in the airway epithelium. 43 In conclusion, the tachykinin NK 1 receptor is involved in the secretory response of goblet cells, [44][45][46][47][48] and we provide evidence for an involvement of this receptor in proliferation of these cells induced by antigen.…”

Section: Discussionmentioning

confidence: 95%

The role of the tachykinin NK1 receptor in airway changes in a mouse model of allergic asthma

Swert

Tournoy

Joos

et al. 2004

Journal of Allergy and Clinical Immunology

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Background: Tachykinins are present in sensory nerves and in nonneuronal cells like macrophages. Human data suggest a role for these peptides in asthma, but the exact role of tachykinins and their receptors in allergic airway inflammation is still a matter of debate. Objective: The aim of this study was to determine the role of the tachykinin NK 1 receptor in allergic airway responses in a mouse model. Methods: Tachykinin NK 1 receptor wild-type and knockout animals were sensitized intraperitoneally to ovalbumin and subsequently exposed from days 14 to 21 to aerosolized ovalbumin (1%). On day 22, the immunologic and histologic changes were evaluated, and lung function measurements were performed. Results: Mice lacking the tachykinin NK 1 receptor and their wild-type litter mates developed inflammatory cell infiltrates in the airways and ovalbumin-specific IgE on sensitization and exposure to ovalbumin compared with saline-exposed controls. No differences were detected between wild-type and knockout mice. The substance P content of alveolar macrophages was not influenced by ovalbumin or by the lack of the NK 1 receptor. Ovalbumin-induced hyperresponsiveness was not observed, but at baseline, the knockout mice were more reactive despite similar morphology. Ovalbumin induced more goblet cell hyperplasia in wild-type animals compared with knockout animals. No differences in airway wall thickness were observed. Conclusion: These data suggest that tachykinin NK 1 receptors do not affect allergic airway inflammation or endogenous substance P content of alveolar macrophages but influence baseline responsiveness and promote features of remodeling such as goblet cell

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“…However, the NK‐1 receptor antagonist CP 96345 did not prevent this type of airway constriction, indicating the specific NK‐2 receptor in mediating the constriction. In addition to airway constriction, released tachykinins cause also coughing and characteristics of neurogenic inflammation, including increases in airway responsiveness ( Girard et al ., 1996 ), plasma extravasation ( Lei et al ., 1996 ; Martling & Lundberg, 1988 ), and airway secretion ( Ramnarine et al ., 1994 ).…”

Section: Discussionmentioning

confidence: 99%

Roles of oxygen radicals and elastase in citric acid‐induced airway constriction of guinea‐pigs

Lai

Chiou

et al. 1999

British J Pharmacology

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1 Antioxidants attenuate noncholinergic airway constriction. To further investigate the relationship between tachykinin-mediated airway constriction and oxygen radicals, we explored citric acidinduced bronchial constriction in 48 young Hartley strain guinea-pigs, divided into six groups: control; citric acid; hexa(sulphobutyl)fullerenes+citric acid; hexa(sulphobutyl)fullerenes+phosphor-amidon+citric acid; dimethylthiourea (DMTU)+citric acid; and DMTU+phosphoramidon+citric acid. Hexa(sulphobutyl)fullerenes and DMTU are scavengers of oxygen radicals while phosphoramidon is an inhibitor of the major degradation enzyme for tachykinins. 2 Animals were anaesthetized, paralyzed, and arti®cially ventilated. Each animal was given 50 breaths of 4 ml saline or citric acid aerosol. We measured dynamic respiratory compliance (Crs), forced expiratory volume in 0.1 (FEV 0.1 ), and maximal expiratory¯ow at 30% total lung capacity (V . max30 ) to evaluate the degree of airway constriction. 3 Citric acid, but not saline, aerosol inhalation caused marked decreases in Crs, FEV 0.1 and V . max30 , indicating marked airway constriction. This constriction was signi®cantly attenuated by either hexa(sulphobutyl)fullerenes or by DMTU. In addition, phosphoramidon signi®cantly reversed the attenuating action of hexa(sulphobutyl)fullerenes, but not that of DMTU. 4 Citric acid aerosol inhalation caused increases in both lucigenin-and t-butyl hydroperoxideinitiated chemiluminescence counts, indicating citric acid-induced increase in oxygen radicals and decrease in antioxidants in bronchoalveolar lavage¯uid. These alterations were signi®cantly suppressed by either hexa(sulphobutyl)fullerenes or DMTU. 5 An elastase inhibitor eglin-c also signi®cantly attenuated citric acid-induced airway constriction, indicating the contributing role of elastase in this type of constriction. 6 We conclude that both oxygen radicals and elastase play an important role in tachykininmediated, citric acid-induced airway constriction.

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‘Sensory‐efferent’ neural control of mucus secretion: characterization using tachykinin receptor antagonists in ferret trachea in vitro

Cited by 44 publications

References 38 publications

Neurogenic inflammation in lung disease: Burnt out?

Neurogenic inflammation in lung disease: Burnt out?

The role of the tachykinin NK1 receptor in airway changes in a mouse model of allergic asthma

Roles of oxygen radicals and elastase in citric acid‐induced airway constriction of guinea‐pigs

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