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Nociceptin inhibits airway microvascular leakage induced by HCl intra-oesophageal instillation.
Br J Pharmacol. 2004 Mar; 141(6):1077-83.BJ

Abstract

1. Gastro-oesophageal acid reflux may cause airway responses such as cough, bronchoconstriction and inflammation in asthmatic patients. Our previous results suggest that microvascular leakage induced, in the guinea-pig airways, by intra-oesophageal hydrochloric acid (HCl) infusion was mainly dependent on the release of tachykinins. Nociceptin, an endogenous ligand of the opioid receptor NOP, has been shown to inhibit bronchoconstriction and cough in guinea-pig or cat by inhibiting tachykinin release. 2. The purpose of this study was to investigate the effects of nociceptin on the intra-oesophageal HCl-induced airway microvascular leakage evaluated by Evans blue dye extravasation measurement in anaesthetised guinea-pigs pretreated with propranolol, atropine and phosphoramidon. 3. Infusion of intra-oesophageal HCl led to a significant increase in plasma extravasation in the main bronchi and trachea. This increase was abolished when animals underwent a bilateral vagotomy. 4. Airway microvascular leakage was inhibited by nociceptin (3-30 microg x kg(-1) i.v.) in a dose-dependent manner (maximal inhibition at the dose of 30 microg x kg(-1): 19.76+/-1.13 vs 90.92+/-14.00 ng x mg(-1) tissue for nociceptin and HCl infusion, respectively, in the main bronchi, P<0.01). The NOP receptor agonist [Arg(14),Lys(15)]N/OFQ mimicked the inhibitory effect of nociceptin, but at a 10-fold lower dose (3 microg x kg(-1) i.v). The NOP receptor antagonist J-113397 had no effect on plasma protein extravasation by itself, but was able to block the inhibitory effect of nociceptin. 5. Morphine (1 mg x kg(-1)) had a similar inhibitory effect as that of nociceptin. Naloxone pretreatment abolished the effect of morphine, but was enable to block the inhibitory effect of nociceptin. 6. Under similar conditions, nociceptin, in the previous range of concentration, was unable to counteract the airway microvascular leakage induced by substance P (SP). 7. These results suggest that airway plasma extravasation induced by intra-oesophageal HCl instillation might be inhibited by specific stimulation of the NOP receptor with nociceptin. Nociceptin is likely to act at a pre-junctional level, by inhibiting tachykinin release, since it was unable to prevent SP-induced airway plasma extravasation.

Authors+Show Affiliations

UPRES EA220 - Pharmacology, University of Versailles and UFR Biomédicale des Saints Pères, 45 rue des Saints Pères, F-75006 Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

14993101

Citation

Rouget, Céline, et al. "Nociceptin Inhibits Airway Microvascular Leakage Induced By HCl Intra-oesophageal Instillation." British Journal of Pharmacology, vol. 141, no. 6, 2004, pp. 1077-83.
Rouget C, Cui YY, D'Agostino B, et al. Nociceptin inhibits airway microvascular leakage induced by HCl intra-oesophageal instillation. Br J Pharmacol. 2004;141(6):1077-83.
Rouget, C., Cui, Y. Y., D'Agostino, B., Faisy, C., Naline, E., Bardou, M., & Advenier, C. (2004). Nociceptin inhibits airway microvascular leakage induced by HCl intra-oesophageal instillation. British Journal of Pharmacology, 141(6), 1077-83.
Rouget C, et al. Nociceptin Inhibits Airway Microvascular Leakage Induced By HCl Intra-oesophageal Instillation. Br J Pharmacol. 2004;141(6):1077-83. PubMed PMID: 14993101.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nociceptin inhibits airway microvascular leakage induced by HCl intra-oesophageal instillation. AU - Rouget,Céline, AU - Cui,Yong Yao, AU - D'Agostino,Bruno, AU - Faisy,Christophe, AU - Naline,Emmanuel, AU - Bardou,Marc, AU - Advenier,Charles, Y1 - 2004/03/01/ PY - 2004/3/3/pubmed PY - 2005/4/12/medline PY - 2004/3/3/entrez SP - 1077 EP - 83 JF - British journal of pharmacology JO - Br. J. Pharmacol. VL - 141 IS - 6 N2 - 1. Gastro-oesophageal acid reflux may cause airway responses such as cough, bronchoconstriction and inflammation in asthmatic patients. Our previous results suggest that microvascular leakage induced, in the guinea-pig airways, by intra-oesophageal hydrochloric acid (HCl) infusion was mainly dependent on the release of tachykinins. Nociceptin, an endogenous ligand of the opioid receptor NOP, has been shown to inhibit bronchoconstriction and cough in guinea-pig or cat by inhibiting tachykinin release. 2. The purpose of this study was to investigate the effects of nociceptin on the intra-oesophageal HCl-induced airway microvascular leakage evaluated by Evans blue dye extravasation measurement in anaesthetised guinea-pigs pretreated with propranolol, atropine and phosphoramidon. 3. Infusion of intra-oesophageal HCl led to a significant increase in plasma extravasation in the main bronchi and trachea. This increase was abolished when animals underwent a bilateral vagotomy. 4. Airway microvascular leakage was inhibited by nociceptin (3-30 microg x kg(-1) i.v.) in a dose-dependent manner (maximal inhibition at the dose of 30 microg x kg(-1): 19.76+/-1.13 vs 90.92+/-14.00 ng x mg(-1) tissue for nociceptin and HCl infusion, respectively, in the main bronchi, P<0.01). The NOP receptor agonist [Arg(14),Lys(15)]N/OFQ mimicked the inhibitory effect of nociceptin, but at a 10-fold lower dose (3 microg x kg(-1) i.v). The NOP receptor antagonist J-113397 had no effect on plasma protein extravasation by itself, but was able to block the inhibitory effect of nociceptin. 5. Morphine (1 mg x kg(-1)) had a similar inhibitory effect as that of nociceptin. Naloxone pretreatment abolished the effect of morphine, but was enable to block the inhibitory effect of nociceptin. 6. Under similar conditions, nociceptin, in the previous range of concentration, was unable to counteract the airway microvascular leakage induced by substance P (SP). 7. These results suggest that airway plasma extravasation induced by intra-oesophageal HCl instillation might be inhibited by specific stimulation of the NOP receptor with nociceptin. Nociceptin is likely to act at a pre-junctional level, by inhibiting tachykinin release, since it was unable to prevent SP-induced airway plasma extravasation. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/14993101/Nociceptin_inhibits_airway_microvascular_leakage_induced_by_HCl_intra_oesophageal_instillation_ L2 - https://doi.org/10.1038/sj.bjp.0705704 DB - PRIME DP - Unbound Medicine ER -