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Involvement of tachykinin NK3 receptors in citric acid-induced cough and bronchial responses in guinea pigs.
Am J Respir Crit Care Med. 1998 Jul; 158(1):42-8.AJ

Abstract

Aerosolized citric acid induces several pulmonary effects including bronchoconstriction, airway inflammation, and cough. Evidence from the use of tachykinin NK1 and NK2 receptor antagonists, as well as chronic treatment with high doses of capsaicin, have suggested that these effects are mediated through the release of tachykinins from sensory nerve endings. In the present study, we have investigated the effects of a tachykinin NK3 receptor antagonist, SR 142801 (osanetant), on cough, bronchoconstriction, and bronchial hyperresponsiveness induced by aerosolized citric acid (0.4 M) in guinea pigs. SR 142801, at 0.3 and 1 mg . kg-1 by intraperitoneal route, significantly inhibited cough in conscious guinea pigs by 57 +/- 3 and 62 +/- 10% (n = 8), respectively. In anaesthetized guinea pigs, it failed to inhibit the bronchoconstriction induced by citric acid when given alone but abolished it when combined with the tachykinin NK2 receptor antagonist, SR 48968 (saredutant). In guinea pigs pretreated with thiorphan (1 mg . kg-1), aerosolized citric acid (0.4 M, 1 h) induced airway hyperresponsiveness 24 h later, displayed by an exaggerated response to the bronchoconstrictor effect of acetylcholine. A microvascular leakage hypersensitivity also occurred and was demonstrated by a potentiation of the plasma protein extravasation from bronchial vessels induced by histamine. When given once intraperitoneally at 1 mg . kg-1 30 min before the citric acid exposure, SR 142801 inhibited both hyperresponsiveness to acetylcholine and the potentiation of histamine-induced increase in microvascular permeability. The results suggest that tachykinin NK3 receptors are involved in citric acid-induced effects on airways.

Authors+Show Affiliations

Laboratoire de Pharmacologie, Faculté de Médecine Paris-Ouest, 15 rue de l'Ecole de Médecine, 75006 Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9655705

Citation

Daoui, S, et al. "Involvement of Tachykinin NK3 Receptors in Citric Acid-induced Cough and Bronchial Responses in Guinea Pigs." American Journal of Respiratory and Critical Care Medicine, vol. 158, no. 1, 1998, pp. 42-8.
Daoui S, Cognon C, Naline E, et al. Involvement of tachykinin NK3 receptors in citric acid-induced cough and bronchial responses in guinea pigs. Am J Respir Crit Care Med. 1998;158(1):42-8.
Daoui, S., Cognon, C., Naline, E., Emonds-Alt, X., & Advenier, C. (1998). Involvement of tachykinin NK3 receptors in citric acid-induced cough and bronchial responses in guinea pigs. American Journal of Respiratory and Critical Care Medicine, 158(1), 42-8.
Daoui S, et al. Involvement of Tachykinin NK3 Receptors in Citric Acid-induced Cough and Bronchial Responses in Guinea Pigs. Am J Respir Crit Care Med. 1998;158(1):42-8. PubMed PMID: 9655705.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of tachykinin NK3 receptors in citric acid-induced cough and bronchial responses in guinea pigs. AU - Daoui,S, AU - Cognon,C, AU - Naline,E, AU - Emonds-Alt,X, AU - Advenier,C, PY - 1998/7/9/pubmed PY - 1998/7/9/medline PY - 1998/7/9/entrez SP - 42 EP - 8 JF - American journal of respiratory and critical care medicine JO - Am J Respir Crit Care Med VL - 158 IS - 1 N2 - Aerosolized citric acid induces several pulmonary effects including bronchoconstriction, airway inflammation, and cough. Evidence from the use of tachykinin NK1 and NK2 receptor antagonists, as well as chronic treatment with high doses of capsaicin, have suggested that these effects are mediated through the release of tachykinins from sensory nerve endings. In the present study, we have investigated the effects of a tachykinin NK3 receptor antagonist, SR 142801 (osanetant), on cough, bronchoconstriction, and bronchial hyperresponsiveness induced by aerosolized citric acid (0.4 M) in guinea pigs. SR 142801, at 0.3 and 1 mg . kg-1 by intraperitoneal route, significantly inhibited cough in conscious guinea pigs by 57 +/- 3 and 62 +/- 10% (n = 8), respectively. In anaesthetized guinea pigs, it failed to inhibit the bronchoconstriction induced by citric acid when given alone but abolished it when combined with the tachykinin NK2 receptor antagonist, SR 48968 (saredutant). In guinea pigs pretreated with thiorphan (1 mg . kg-1), aerosolized citric acid (0.4 M, 1 h) induced airway hyperresponsiveness 24 h later, displayed by an exaggerated response to the bronchoconstrictor effect of acetylcholine. A microvascular leakage hypersensitivity also occurred and was demonstrated by a potentiation of the plasma protein extravasation from bronchial vessels induced by histamine. When given once intraperitoneally at 1 mg . kg-1 30 min before the citric acid exposure, SR 142801 inhibited both hyperresponsiveness to acetylcholine and the potentiation of histamine-induced increase in microvascular permeability. The results suggest that tachykinin NK3 receptors are involved in citric acid-induced effects on airways. SN - 1073-449X UR - https://www.unboundmedicine.com/medline/citation/9655705/Involvement_of_tachykinin_NK3_receptors_in_citric_acid_induced_cough_and_bronchial_responses_in_guinea_pigs_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm.158.1.9705052?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -