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Activation of the nociceptin/orphanin FQ receptor reduces bronchoconstriction and microvascular leakage in a rabbit model of gastroesophageal reflux.
Br J Pharmacol. 2005 Mar; 144(6):813-20.BJ

Abstract

1. Nociceptin/orphanin FQ (N/OFQ) is the endogenous peptide ligand for a specific G-protein coupled receptor, the N/OFQ peptide receptor (NOP). The N/OFQ-NOP receptor system has been reported to play an important role in pain, anxiety and appetite regulation. In airways, N/OFQ was found to inhibit the release of tachykinins and the bronchoconstriction and cough provoked by capsaicin. 2. Here we evaluated the effects of NOP receptor activation in bronchoconstriction and airway microvascular leakage induced by intraesophageal (i.oe.) hydrochloric acid (HCl) instillation in rabbits. We also tested the effects of NOP receptor activation in SP-induced plasma extravasation and bronchoconstriction. 3. In anesthetized New Zealand rabbits bronchopulmonary function (total lung resistance (R(L)) and dynamic compliance (C(dyn))) and airway microvascular leakage (extravasation of Evans blue dye) were evaluated. 4. Infusion of i.oe. HCl (1 N) led to a significant increase in bronchoconstriction and plasma extravasation in the main bronchi and trachea of rabbits pretreated with propranolol, atropine and phosphoramidon. 5. Bronchoconstriction and airway microvascular leakage were inhibited by N/OFQ (3-30 microg kg(-1) i.v.) in a dose-dependent manner. The NOP receptor agonist [Arg14,Lys15]N/OFQ mimicked the inhibitory effect of N/OFQ, being 10-fold more potent, UFP-101, a peptide selective NOP receptor antagonist, blocked the inhibitory effects of both agonists. 6. Under the same experimental conditions, N/OFQ and [Arg14,Lys15]N/OFQ did not counteract the bronchoconstriction and airway microvascular leakage induced by substance P. 7. These results suggest that bronchoconstriction and airway plasma extravasation induced by i.oe. HCl instillation are inhibited by activation of prejunctional NOP receptors.

Authors+Show Affiliations

Department of Experimental Medicine-Section of Pharmacology, Faculty of Medicine and Surgery, 2nd University of Naples, via Constantinopoli 16, 80138 Naples, Italy. bruno.dagostino@unina2.itNo affiliation info availableNo 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

15685213

Citation

D'Agostino, Bruno, et al. "Activation of the Nociceptin/orphanin FQ Receptor Reduces Bronchoconstriction and Microvascular Leakage in a Rabbit Model of Gastroesophageal Reflux." British Journal of Pharmacology, vol. 144, no. 6, 2005, pp. 813-20.
D'Agostino B, Marrocco G, De Nardo M, et al. Activation of the nociceptin/orphanin FQ receptor reduces bronchoconstriction and microvascular leakage in a rabbit model of gastroesophageal reflux. Br J Pharmacol. 2005;144(6):813-20.
D'Agostino, B., Marrocco, G., De Nardo, M., Calò, G., Guerrini, R., Gallelli, L., Advenier, C., & Rossi, F. (2005). Activation of the nociceptin/orphanin FQ receptor reduces bronchoconstriction and microvascular leakage in a rabbit model of gastroesophageal reflux. British Journal of Pharmacology, 144(6), 813-20.
D'Agostino B, et al. Activation of the Nociceptin/orphanin FQ Receptor Reduces Bronchoconstriction and Microvascular Leakage in a Rabbit Model of Gastroesophageal Reflux. Br J Pharmacol. 2005;144(6):813-20. PubMed PMID: 15685213.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of the nociceptin/orphanin FQ receptor reduces bronchoconstriction and microvascular leakage in a rabbit model of gastroesophageal reflux. AU - D'Agostino,Bruno, AU - Marrocco,Giuseppina, AU - De Nardo,Marilisa, AU - Calò,Girolamo, AU - Guerrini,Remo, AU - Gallelli,Luca, AU - Advenier,Charles, AU - Rossi,Francesco, PY - 2005/2/3/pubmed PY - 2005/7/15/medline PY - 2005/2/3/entrez SP - 813 EP - 20 JF - British journal of pharmacology JO - Br. J. Pharmacol. VL - 144 IS - 6 N2 - 1. Nociceptin/orphanin FQ (N/OFQ) is the endogenous peptide ligand for a specific G-protein coupled receptor, the N/OFQ peptide receptor (NOP). The N/OFQ-NOP receptor system has been reported to play an important role in pain, anxiety and appetite regulation. In airways, N/OFQ was found to inhibit the release of tachykinins and the bronchoconstriction and cough provoked by capsaicin. 2. Here we evaluated the effects of NOP receptor activation in bronchoconstriction and airway microvascular leakage induced by intraesophageal (i.oe.) hydrochloric acid (HCl) instillation in rabbits. We also tested the effects of NOP receptor activation in SP-induced plasma extravasation and bronchoconstriction. 3. In anesthetized New Zealand rabbits bronchopulmonary function (total lung resistance (R(L)) and dynamic compliance (C(dyn))) and airway microvascular leakage (extravasation of Evans blue dye) were evaluated. 4. Infusion of i.oe. HCl (1 N) led to a significant increase in bronchoconstriction and plasma extravasation in the main bronchi and trachea of rabbits pretreated with propranolol, atropine and phosphoramidon. 5. Bronchoconstriction and airway microvascular leakage were inhibited by N/OFQ (3-30 microg kg(-1) i.v.) in a dose-dependent manner. The NOP receptor agonist [Arg14,Lys15]N/OFQ mimicked the inhibitory effect of N/OFQ, being 10-fold more potent, UFP-101, a peptide selective NOP receptor antagonist, blocked the inhibitory effects of both agonists. 6. Under the same experimental conditions, N/OFQ and [Arg14,Lys15]N/OFQ did not counteract the bronchoconstriction and airway microvascular leakage induced by substance P. 7. These results suggest that bronchoconstriction and airway plasma extravasation induced by i.oe. HCl instillation are inhibited by activation of prejunctional NOP receptors. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/15685213/Activation_of_the_nociceptin/orphanin_FQ_receptor_reduces_bronchoconstriction_and_microvascular_leakage_in_a_rabbit_model_of_gastroesophageal_reflux_ L2 - https://doi.org/10.1038/sj.bjp.0706066 DB - PRIME DP - Unbound Medicine ER -