ArticleBritish journal of pharmacology2003
Tachykinin NK3 and NK1 receptor activation elicits secretion from porcine airway submucosal glands.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- PAR-2-activated secretion by airway gland serous cells: role for CFTR and inhibition byAmerican journal of physiology. Lung cellular and molecular physiology · 2021Article
- Overexpression of Substance P in pig airways increases MUC5AC through an NF-kβ pathway.Physiological reports · 2021Article
- Neuropeptides in asthma, chronic obstructive pulmonary disease and cystic fibrosis.Respiratory research · 2018Review
- Substance P stimulates human airway submucosal gland secretion mainly via a CFTR-dependent process.The Journal of clinical investigation · 2009Article
- Substance P stimulates CFTR-dependent fluid secretion by mouse tracheal submucosal glands.Pflugers Archiv : European journal of physiology · 2008Article
- Fluid secretion by submucosal glands of the tracheobronchial airways.Respiratory physiology & neurobiology · 2007Review
- Parasympathetic control of airway submucosal glands: central reflexes and the airway intrinsic nervous system.Autonomic neuroscience : basic & clinical · 2007Review
- Mucus secretion by single tracheal submucosal glands from normal and cystic fibrosis transmembrane conductance regulator knockout mice.The Journal of physiology · 2007Article
- Liquid secretion properties of airway submucosal glands.The Journal of physiology · 2004Review
- Cellular and molecular mechanisms in environmental and occupational inhalation toxicology.GMS current topics in otorhinolaryngology, head and neck surgery · 2004Article
- Mechanisms underlying the inhibitory effects of tachykinin receptor antagonists on eosinophil recruitment in an allergic pleurisy model in mice.British journal of pharmacology · 2003Article
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1 We presently characterized the tachykinin receptor subtypes, using tachykinin receptor agonists and selective antagonists, that induce submucosal gland fluid flux (J(G)) from porcine tracheal explants with the hillocks technique. We also investigated the effects of the tachykinin receptor agonists on the electrophysiologic parameters of the tracheal epithelium in Ussing chambers. 2 The NK(1) tachykinin receptor agonist substance P (SP, 1 microM) and the NK(3) tachykinin receptor agonist [MePhe(7)]neurokinin B ([MePhe(7)]NKB, 1 microM) induced gland fluid fluxes of 0.29+/-0.03 microl min(-1) cm(-2) (n=26) and 0.36+/-0.05 microl min(-1) cm(-2) (n=24), respectively; while the NK(2) tachykinin receptor agonist [betaAla(8)]neurokinin A (4-10) ([betaAla(8)]NKA (4-10), 1 microM) had no effect on J(G) (n=10). 3 The NK(1) receptor antagonist CP99994 (1 microM, n=9) blocked 93% of the SP-induced J(G), whereas the NK(3) receptor antagonist SB223412 (1 microM, n=12) had no effect on the SP-induced J(G). However, SB223412 (1 microM, n=9) blocked 89% of the [MePhe(7)]NKB-induced J(G) while CP99994 (1 microM, n=10) did not affect the [MePhe(7)]NKB-induced J(G). The NK(2) receptor antagonist SR48968 (1 microM) did not block the J(G) induced by either the NK(1) (n=4) or NK(3) (n=13) receptor agonists. 4 The nicotinic ganglionic acetylcholine receptor antagonist hexamethonium (1 microM) and the muscarinic acetylcholine receptor antagonist atropine (1 microM) also decreased the NK(3) receptor agonist-induced J(G) by 67% (n=10) and 71% (n=12), respectively. 5 The potential difference (PD), short-circuit current (I(SC)), and membrane resistance (R(M)) of the porcine tracheal epithelial membranes were not significantly affected by any of the neurokinin agonists or antagonists (1 microM, basolateral) used in this study, although SP and [betaAla(8)]NKA (4-10) induced a slight transient epithelial hyperpolarization. 6 These data suggest that NK(1) and NK(3) receptors induce porcine airway gland secretion by different mechanisms and that the NK(3) receptor agonists induced secretion is likely due to activation of prejunctional NK(3) receptors on parasympathetic nerves, resulting in acetylcholine-release. We conclude that tachykinin receptor antagonists may have therapeutic potential in diseases with pathophysiological mucus hypersecretion such as asthma and chronic bronchitis.
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