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TRPV1 controls acid- and heat-induced calcitonin gene-related peptide release and sensitization by bradykinin in the isolated mouse trachea.
Eur J Neurosci. 2009 May; 29(9):1896-904.EJ

Abstract

Chronic cough derives from inflammatory hypersensitivity of tracheobronchial nerve endings, most of which express the polymodal capsaicin receptor-channel transient receptor potential vanilloid (TRPV) type 1 and the secretory neuropeptide calcitonin gene-related peptide (CGRP). An isolated mouse trachea preparation was established to measure chemically and thermally stimulated CGRP release as an index for sensory transduction of potential cough-inducing stimuli. TRPV1 knockout mice were employed to assess the TRPV1 contribution to tracheal responsiveness and sensitization. Graded heat-induced CGRP release depended entirely on extracellular calcium and partly on TRPV1; knockout mice showed 60% less CGRP release at 45 degrees C (for 5 min) than wild-types. This heat response was facilitated by the TRPV1 agonist ethanol and the TRPV1-3 agonist 2-aminoethoxydiphenyl borate, effects that were reduced or absent in TRPV1(-/-), respectively. The TRPV1 antagonists ruthenium red and N-(4-t-butylphenyl)-4-(3-chloropyridin-2-yl) tetrahydropyrazine-1(2H)-carboxamide were ineffective on the basal heat response. A step increase of temperature from 22 to 40 degrees C caused a TRPV1-independent CGRP release that was doubled by bradykinin in wild-types but not TRPV1(-/-). Proton stimulation resulted in a bell-shaped concentration-response curve with threshold at pH 6.7 and a maximum at pH 5.7; responses were greatly reduced but not abolished in TRPV1(-/-). Coadministration of amiloride (30 microm), the blocker of acid-sensing ion channels, was ineffective in both TRPV1 genotypes. The data suggest that tracheal acid sensing mainly involves TRPV1 but not acid-sensing ion channels, whereas noxious heat responsiveness partly depends and (inflammatory) sensitization to heat largely depends on the capsaicin receptor in tracheal nerve endings. Lowering of their heat threshold to near body temperature may sustain hypersensitivity and neurogenic inflammation of the upper airways.

Authors+Show Affiliations

Department of Physiology and Pathophysiology, University of Erlangen-Nuremberg, Erlangen, Germany. kichko@physiologie1.uni-erlangen.deNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19473241

Citation

Kichko, Tatjana I., and Peter W. Reeh. "TRPV1 Controls Acid- and Heat-induced Calcitonin Gene-related Peptide Release and Sensitization By Bradykinin in the Isolated Mouse Trachea." The European Journal of Neuroscience, vol. 29, no. 9, 2009, pp. 1896-904.
Kichko TI, Reeh PW. TRPV1 controls acid- and heat-induced calcitonin gene-related peptide release and sensitization by bradykinin in the isolated mouse trachea. Eur J Neurosci. 2009;29(9):1896-904.
Kichko, T. I., & Reeh, P. W. (2009). TRPV1 controls acid- and heat-induced calcitonin gene-related peptide release and sensitization by bradykinin in the isolated mouse trachea. The European Journal of Neuroscience, 29(9), 1896-904. https://doi.org/10.1111/j.1460-9568.2009.06747.x
Kichko TI, Reeh PW. TRPV1 Controls Acid- and Heat-induced Calcitonin Gene-related Peptide Release and Sensitization By Bradykinin in the Isolated Mouse Trachea. Eur J Neurosci. 2009;29(9):1896-904. PubMed PMID: 19473241.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - TRPV1 controls acid- and heat-induced calcitonin gene-related peptide release and sensitization by bradykinin in the isolated mouse trachea. AU - Kichko,Tatjana I, AU - Reeh,Peter W, Y1 - 2009/04/17/ PY - 2009/5/29/entrez PY - 2009/5/29/pubmed PY - 2009/8/21/medline SP - 1896 EP - 904 JF - The European journal of neuroscience JO - Eur J Neurosci VL - 29 IS - 9 N2 - Chronic cough derives from inflammatory hypersensitivity of tracheobronchial nerve endings, most of which express the polymodal capsaicin receptor-channel transient receptor potential vanilloid (TRPV) type 1 and the secretory neuropeptide calcitonin gene-related peptide (CGRP). An isolated mouse trachea preparation was established to measure chemically and thermally stimulated CGRP release as an index for sensory transduction of potential cough-inducing stimuli. TRPV1 knockout mice were employed to assess the TRPV1 contribution to tracheal responsiveness and sensitization. Graded heat-induced CGRP release depended entirely on extracellular calcium and partly on TRPV1; knockout mice showed 60% less CGRP release at 45 degrees C (for 5 min) than wild-types. This heat response was facilitated by the TRPV1 agonist ethanol and the TRPV1-3 agonist 2-aminoethoxydiphenyl borate, effects that were reduced or absent in TRPV1(-/-), respectively. The TRPV1 antagonists ruthenium red and N-(4-t-butylphenyl)-4-(3-chloropyridin-2-yl) tetrahydropyrazine-1(2H)-carboxamide were ineffective on the basal heat response. A step increase of temperature from 22 to 40 degrees C caused a TRPV1-independent CGRP release that was doubled by bradykinin in wild-types but not TRPV1(-/-). Proton stimulation resulted in a bell-shaped concentration-response curve with threshold at pH 6.7 and a maximum at pH 5.7; responses were greatly reduced but not abolished in TRPV1(-/-). Coadministration of amiloride (30 microm), the blocker of acid-sensing ion channels, was ineffective in both TRPV1 genotypes. The data suggest that tracheal acid sensing mainly involves TRPV1 but not acid-sensing ion channels, whereas noxious heat responsiveness partly depends and (inflammatory) sensitization to heat largely depends on the capsaicin receptor in tracheal nerve endings. Lowering of their heat threshold to near body temperature may sustain hypersensitivity and neurogenic inflammation of the upper airways. SN - 1460-9568 UR - https://www.unboundmedicine.com/medline/citation/19473241/TRPV1_controls_acid__and_heat_induced_calcitonin_gene_related_peptide_release_and_sensitization_by_bradykinin_in_the_isolated_mouse_trachea_ L2 - https://doi.org/10.1111/j.1460-9568.2009.06747.x DB - PRIME DP - Unbound Medicine ER -