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Nociceptin/orphanin FQ inhibits capsaicin-induced guinea-pig airway contraction through an inward-rectifier potassium channel.
Br J Pharmacol. 2002 Feb; 135(3):764-70.BJ

Abstract

Nociceptin/orphanin FQ (N/OFQ), an endogenous opioid-like orphan receptor (NOP receptor, previously termed ORL1 receptor) agonist, has been found to inhibit capsaicin-induced bronchoconstriction in isolated guinea-pig lungs and in vivo. The underlying mechanisms are not clear. In the present studies, we tested the effect of N/OFQ on VR1 channel function in isolated guinea-pig nodose ganglia cells. Capsaicin increased intracellular Ca(2+) concentration in these cells through activation of vanilloid receptors. Capsaicin-induced Ca(2+) responses were attenuated by pretreatment of nodose neurons with N/OFQ (1 microM). N/OFQ inhibitory effect on the Ca(2+) response in nodose ganglia cells was antagonized by tertiapin (0.5 microM), an inhibitor of inward-rectifier K(+) channels, but not by verapamil, a voltage gated Ca(2+) channel blocker, indicating that an inward-rectifier K(+) channel is involved in N/OFQ inhibitory effect. In isolated guinea-pig bronchus, N/OFQ (1 microM) inhibited capsaicin-induced airway contraction. Tertiapin (0.5 microM) abolished the N/OFQ inhibition of capsaicin-induced bronchial contraction. Capsaicin (10 microg) increased pulmonary inflation pressure in the isolated perfused guinea-pig lungs. This response was significantly attenuated by pretreatment with N/OFQ (1 microM). Tertiapin also abolished the N/OFQ inhibitory effect on capsaicin-induced bronchoconstriction in perfused lungs. Capsaicin increased the release of substance P and neurokinin A from isolated lungs. N/OFQ (1 microM) blocked the capsaicin-induced tachykinin release. These results indicate that N/OFQ-induced hyperpolarization of tachykinin containing airway sensory nerves, through an inward-rectifier K(+) channel activation, accounts for the inhibition of capsaicin-evoked broncoconstriction.

Authors+Show Affiliations

Allergy, Schering-Plough Research Institute, Kenilworth, New Jersey 07033, USA. yanlin.jia@spcorp.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11834624

Citation

Jia, Yanlin, et al. "Nociceptin/orphanin FQ Inhibits Capsaicin-induced Guinea-pig Airway Contraction Through an Inward-rectifier Potassium Channel." British Journal of Pharmacology, vol. 135, no. 3, 2002, pp. 764-70.
Jia Y, Wang X, Aponte SI, et al. Nociceptin/orphanin FQ inhibits capsaicin-induced guinea-pig airway contraction through an inward-rectifier potassium channel. Br J Pharmacol. 2002;135(3):764-70.
Jia, Y., Wang, X., Aponte, S. I., Rivelli, M. A., Yang, R., Rizzo, C. A., Corboz, M. R., Priestley, T., & Hey, J. A. (2002). Nociceptin/orphanin FQ inhibits capsaicin-induced guinea-pig airway contraction through an inward-rectifier potassium channel. British Journal of Pharmacology, 135(3), 764-70.
Jia Y, et al. Nociceptin/orphanin FQ Inhibits Capsaicin-induced Guinea-pig Airway Contraction Through an Inward-rectifier Potassium Channel. Br J Pharmacol. 2002;135(3):764-70. PubMed PMID: 11834624.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nociceptin/orphanin FQ inhibits capsaicin-induced guinea-pig airway contraction through an inward-rectifier potassium channel. AU - Jia,Yanlin, AU - Wang,Xin, AU - Aponte,Sonia I, AU - Rivelli,Maria A, AU - Yang,Richard, AU - Rizzo,Charles A, AU - Corboz,Michel R, AU - Priestley,Tony, AU - Hey,John A, PY - 2002/2/9/pubmed PY - 2002/5/22/medline PY - 2002/2/9/entrez SP - 764 EP - 70 JF - British journal of pharmacology JO - Br. J. Pharmacol. VL - 135 IS - 3 N2 - Nociceptin/orphanin FQ (N/OFQ), an endogenous opioid-like orphan receptor (NOP receptor, previously termed ORL1 receptor) agonist, has been found to inhibit capsaicin-induced bronchoconstriction in isolated guinea-pig lungs and in vivo. The underlying mechanisms are not clear. In the present studies, we tested the effect of N/OFQ on VR1 channel function in isolated guinea-pig nodose ganglia cells. Capsaicin increased intracellular Ca(2+) concentration in these cells through activation of vanilloid receptors. Capsaicin-induced Ca(2+) responses were attenuated by pretreatment of nodose neurons with N/OFQ (1 microM). N/OFQ inhibitory effect on the Ca(2+) response in nodose ganglia cells was antagonized by tertiapin (0.5 microM), an inhibitor of inward-rectifier K(+) channels, but not by verapamil, a voltage gated Ca(2+) channel blocker, indicating that an inward-rectifier K(+) channel is involved in N/OFQ inhibitory effect. In isolated guinea-pig bronchus, N/OFQ (1 microM) inhibited capsaicin-induced airway contraction. Tertiapin (0.5 microM) abolished the N/OFQ inhibition of capsaicin-induced bronchial contraction. Capsaicin (10 microg) increased pulmonary inflation pressure in the isolated perfused guinea-pig lungs. This response was significantly attenuated by pretreatment with N/OFQ (1 microM). Tertiapin also abolished the N/OFQ inhibitory effect on capsaicin-induced bronchoconstriction in perfused lungs. Capsaicin increased the release of substance P and neurokinin A from isolated lungs. N/OFQ (1 microM) blocked the capsaicin-induced tachykinin release. These results indicate that N/OFQ-induced hyperpolarization of tachykinin containing airway sensory nerves, through an inward-rectifier K(+) channel activation, accounts for the inhibition of capsaicin-evoked broncoconstriction. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/11834624/Nociceptin/orphanin_FQ_inhibits_capsaicin_induced_guinea_pig_airway_contraction_through_an_inward_rectifier_potassium_channel_ L2 - https://doi.org/10.1038/sj.bjp.0704515 DB - PRIME DP - Unbound Medicine ER -