The bitter taste receptor (TAS2R) agonists denatonium and chloroquine display distinct patterns of relaxation of the guinea pig trachea
Identifieur interne : 000005 ( PascalFrancis/Corpus ); précédent : 000004; suivant : 000006The bitter taste receptor (TAS2R) agonists denatonium and chloroquine display distinct patterns of relaxation of the guinea pig trachea
Auteurs : Ville Pulkkinen ; Martijn L. Manson ; Jesper Safholm ; Mikael Adner ; Sven-Erik DahlenSource :
- American journal of physiology. Lung cellular and molecular physiology [ 1040-0605 ] ; 2012.
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Abstract
Activation of taste receptors (TAS2Rs) by bitter taste agonists has been reported to cause bronchodilation. The aim of this study was to extend the information on the effects of bitter taste agonists on responses induced by different contractile mediators in a standard airway physiology preparation. Isometric responses were assessed in guinea pig trachea (GPT). TAS2R agonists were administered either to segments precontracted with different agonists for contraction or given before challenge with the different contractile stimuli, including antigen in tissues from ovalbumin-sensitized animals. TAS2R mRNA expression on GPT epithelium and smooth muscle was measured with real-time PCR. Denatonium, chloroquine, thiamine, and noscapine induced concentration-dependent relaxations (Rmax: 98.3 ± 1.6, 100.0 ± 0.0, 100.0 ± 0.0, and 52.3 ± 1.1% of maximum, respectively, in the presence of indomethacin) in segments precontracted with carbachol. The receptors for denatonium (TAS2R4, TAS2R10) and chloroquine (TAS2R3, TAS2R10) were expressed in GPT. Whereas denatonium selectively inhibited contractions induced by carbachol, chloroquine uniformly inhibited contractions evoked by prostaglandin E2, the thromboxane receptor agonist U-46619, leukotriene D4, histamine, and antigen. The effects of denatonium, but not those of chloroquine, were partly inhibited by blockers of the large Ca2+-activated K+ channels and decreased by an increase of the level of precontraction. In conclusion, TAS2R agonists mediated strong relaxations and substantial inhibition of contractions in GPT. Chloroquine and denatonium had distinct patterns of activity, indicating different signaling mechanisms. The findings reinforce the hypothesis that TAS2Rs are potential targets for the development of a new class of more efficacious agonists for bronchodilation.
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Format Inist (serveur)
| NO : | PASCAL 13-0101069 INIST |
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| ET : | The bitter taste receptor (TAS2R) agonists denatonium and chloroquine display distinct patterns of relaxation of the guinea pig trachea |
| AU : | PULKKINEN (Ville); MANSON (Martijn L.); SAFHOLM (Jesper); ADNER (Mikael); DAHLEN (Sven-Erik) |
| AF : | The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet/Stockholm/Suède (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.); Research Programs Unit, Department of Medical Genetics, University of Helsinki/Finlande (1 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | American journal of physiology. Lung cellular and molecular physiology; ISSN 1040-0605; Coden APLPE7; Etats-Unis; Da. 2012; Vol. 47; No. 6; L956-L966; Bibl. 28 ref. |
| LA : | Anglais |
| EA : | Activation of taste receptors (TAS2Rs) by bitter taste agonists has been reported to cause bronchodilation. The aim of this study was to extend the information on the effects of bitter taste agonists on responses induced by different contractile mediators in a standard airway physiology preparation. Isometric responses were assessed in guinea pig trachea (GPT). TAS2R agonists were administered either to segments precontracted with different agonists for contraction or given before challenge with the different contractile stimuli, including antigen in tissues from ovalbumin-sensitized animals. TAS2R mRNA expression on GPT epithelium and smooth muscle was measured with real-time PCR. Denatonium, chloroquine, thiamine, and noscapine induced concentration-dependent relaxations (Rmax: 98.3 ± 1.6, 100.0 ± 0.0, 100.0 ± 0.0, and 52.3 ± 1.1% of maximum, respectively, in the presence of indomethacin) in segments precontracted with carbachol. The receptors for denatonium (TAS2R4, TAS2R10) and chloroquine (TAS2R3, TAS2R10) were expressed in GPT. Whereas denatonium selectively inhibited contractions induced by carbachol, chloroquine uniformly inhibited contractions evoked by prostaglandin E2, the thromboxane receptor agonist U-46619, leukotriene D4, histamine, and antigen. The effects of denatonium, but not those of chloroquine, were partly inhibited by blockers of the large Ca2+-activated K+ channels and decreased by an increase of the level of precontraction. In conclusion, TAS2R agonists mediated strong relaxations and substantial inhibition of contractions in GPT. Chloroquine and denatonium had distinct patterns of activity, indicating different signaling mechanisms. The findings reinforce the hypothesis that TAS2Rs are potential targets for the development of a new class of more efficacious agonists for bronchodilation. |
| CC : | 002A20; 002B11B |
| FD : | Saveur; Récepteur biologique; Agoniste; Chloroquine; Relaxation; Trachée; Bronchodilatation; Asthme; Prostaglandine; Voie respiratoire; Muscle lisse; Mammalia; Cobaye; Appareil respiratoire |
| FG : | Vertebrata; Gustation; Système gustatif; Pathologie de l'appareil respiratoire; Bronchopneumopathie obstructive; Dérivé de l'acide arachidonique; Eicosanoïde; Pathologie des bronches; Pathologie des poumons; Rodentia |
| ED : | Taste; Biological receptor; Agonist; Chloroquine; Relaxation; Trachea; Bronchodilation; Asthma; Prostaglandin; Respiratory tract; Smooth muscle; Mammalia; Guinea pig; Respiratory system |
| EG : | Vertebrata; Gustation; Gustative system; Respiratory disease; Obstructive pulmonary disease; Arachidonic acid derivatives; Eicosanoid; Bronchus disease; Lung disease; Rodentia |
| SD : | Sabor; Receptor biológico; Agonista; Cloroquina; Relajación; Tráquea; Broncodilatación; Asma; Prostaglandina; Vía respiratoria; Músculo liso; Mammalia; Cobayo; Aparato respiratorio |
| LO : | INIST-22200.354000182550680030 |
| ID : | 13-0101069 |
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Manson</name><affiliation><inist:fA14 i1="01"><s1>The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet</s1><s2>Stockholm</s2><s3>SWE</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Safholm, Jesper" sort="Safholm, Jesper" uniqKey="Safholm J" first="Jesper" last="Safholm">Jesper Safholm</name><affiliation><inist:fA14 i1="01"><s1>The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet</s1><s2>Stockholm</s2><s3>SWE</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Adner, Mikael" sort="Adner, Mikael" uniqKey="Adner M" first="Mikael" last="Adner">Mikael Adner</name><affiliation><inist:fA14 i1="01"><s1>The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet</s1><s2>Stockholm</s2><s3>SWE</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Dahlen, Sven Erik" sort="Dahlen, Sven Erik" uniqKey="Dahlen S" first="Sven-Erik" last="Dahlen">Sven-Erik Dahlen</name><affiliation><inist:fA14 i1="01"><s1>The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet</s1><s2>Stockholm</s2><s3>SWE</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">American journal of physiology. Lung cellular and molecular physiology</title><title level="j" type="abbreviated">Am. j. physiol., Lung cell. mol. physiol.</title><idno type="ISSN">1040-0605</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of physiology. Lung cellular and molecular physiology</title><title level="j" type="abbreviated">Am. j. physiol., Lung cell. mol. physiol.</title><idno type="ISSN">1040-0605</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Agonist</term><term>Asthma</term><term>Biological receptor</term><term>Bronchodilation</term><term>Chloroquine</term><term>Guinea pig</term><term>Mammalia</term><term>Prostaglandin</term><term>Relaxation</term><term>Respiratory system</term><term>Respiratory tract</term><term>Smooth muscle</term><term>Taste</term><term>Trachea</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Saveur</term><term>Récepteur biologique</term><term>Agoniste</term><term>Chloroquine</term><term>Relaxation</term><term>Trachée</term><term>Bronchodilatation</term><term>Asthme</term><term>Prostaglandine</term><term>Voie respiratoire</term><term>Muscle lisse</term><term>Mammalia</term><term>Cobaye</term><term>Appareil respiratoire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Activation of taste receptors (TAS2Rs) by bitter taste agonists has been reported to cause bronchodilation. The aim of this study was to extend the information on the effects of bitter taste agonists on responses induced by different contractile mediators in a standard airway physiology preparation. Isometric responses were assessed in guinea pig trachea (GPT). TAS2R agonists were administered either to segments precontracted with different agonists for contraction or given before challenge with the different contractile stimuli, including antigen in tissues from ovalbumin-sensitized animals. TAS2R mRNA expression on GPT epithelium and smooth muscle was measured with real-time PCR. Denatonium, chloroquine, thiamine, and noscapine induced concentration-dependent relaxations (R<sub>max</sub>: 98.3 ± 1.6, 100.0 ± 0.0, 100.0 ± 0.0, and 52.3 ± 1.1% of maximum, respectively, in the presence of indomethacin) in segments precontracted with carbachol. The receptors for denatonium (TAS2R4, TAS2R10) and chloroquine (TAS2R3, TAS2R10) were expressed in GPT. Whereas denatonium selectively inhibited contractions induced by carbachol, chloroquine uniformly inhibited contractions evoked by prostaglandin E<sub>2</sub>, the thromboxane receptor agonist U-46619, leukotriene D<sub>4</sub>, histamine, and antigen. The effects of denatonium, but not those of chloroquine, were partly inhibited by blockers of the large Ca<sup>2+</sup>-activated K<sup>+</sup> channels and decreased by an increase of the level of precontraction. In conclusion, TAS2R agonists mediated strong relaxations and substantial inhibition of contractions in GPT. Chloroquine and denatonium had distinct patterns of activity, indicating different signaling mechanisms. The findings reinforce the hypothesis that TAS2Rs are potential targets for the development of a new class of more efficacious agonists for bronchodilation.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>1040-0605</s0></fA01><fA02 i1="01"><s0>APLPE7</s0></fA02><fA03 i2="1"><s0>Am. j. physiol., Lung cell. mol. physiol.</s0></fA03><fA05><s2>47</s2></fA05><fA06><s2>6</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>The bitter taste receptor (TAS2R) agonists denatonium and chloroquine display distinct patterns of relaxation of the guinea pig trachea</s1></fA08><fA11 i1="01" i2="1"><s1>PULKKINEN (Ville)</s1></fA11><fA11 i1="02" i2="1"><s1>MANSON (Martijn L.)</s1></fA11><fA11 i1="03" i2="1"><s1>SAFHOLM (Jesper)</s1></fA11><fA11 i1="04" i2="1"><s1>ADNER (Mikael)</s1></fA11><fA11 i1="05" i2="1"><s1>DAHLEN (Sven-Erik)</s1></fA11><fA14 i1="01"><s1>The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet</s1><s2>Stockholm</s2><s3>SWE</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Research Programs Unit, Department of Medical Genetics, University of Helsinki</s1><s3>FIN</s3><sZ>1 aut.</sZ></fA14><fA20><s2>L956-L966</s2></fA20><fA21><s1>2012</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>22200</s2><s5>354000182550680030</s5></fA43><fA44><s0>0000</s0><s1>© 2013 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>28 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>13-0101069</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>American journal of physiology. Lung cellular and molecular physiology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Activation of taste receptors (TAS2Rs) by bitter taste agonists has been reported to cause bronchodilation. The aim of this study was to extend the information on the effects of bitter taste agonists on responses induced by different contractile mediators in a standard airway physiology preparation. Isometric responses were assessed in guinea pig trachea (GPT). TAS2R agonists were administered either to segments precontracted with different agonists for contraction or given before challenge with the different contractile stimuli, including antigen in tissues from ovalbumin-sensitized animals. TAS2R mRNA expression on GPT epithelium and smooth muscle was measured with real-time PCR. Denatonium, chloroquine, thiamine, and noscapine induced concentration-dependent relaxations (R<sub>max</sub>: 98.3 ± 1.6, 100.0 ± 0.0, 100.0 ± 0.0, and 52.3 ± 1.1% of maximum, respectively, in the presence of indomethacin) in segments precontracted with carbachol. The receptors for denatonium (TAS2R4, TAS2R10) and chloroquine (TAS2R3, TAS2R10) were expressed in GPT. Whereas denatonium selectively inhibited contractions induced by carbachol, chloroquine uniformly inhibited contractions evoked by prostaglandin E<sub>2</sub>, the thromboxane receptor agonist U-46619, leukotriene D<sub>4</sub>, histamine, and antigen. The effects of denatonium, but not those of chloroquine, were partly inhibited by blockers of the large Ca<sup>2+</sup>-activated K<sup>+</sup> channels and decreased by an increase of the level of precontraction. In conclusion, TAS2R agonists mediated strong relaxations and substantial inhibition of contractions in GPT. Chloroquine and denatonium had distinct patterns of activity, indicating different signaling mechanisms. The findings reinforce the hypothesis that TAS2Rs are potential targets for the development of a new class of more efficacious agonists for bronchodilation.</s0></fC01><fC02 i1="01" i2="X"><s0>002A20</s0></fC02><fC02 i1="02" i2="X"><s0>002B11B</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Saveur</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Taste</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Sabor</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Récepteur biologique</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Biological receptor</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Receptor biológico</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Agoniste</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Agonist</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Agonista</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Chloroquine</s0><s2>NK</s2><s2>FR</s2><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Chloroquine</s0><s2>NK</s2><s2>FR</s2><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Cloroquina</s0><s2>NK</s2><s2>FR</s2><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Relaxation</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Relaxation</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Relajación</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Trachée</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Trachea</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Tráquea</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Bronchodilatation</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Bronchodilation</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Broncodilatación</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Asthme</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Asthma</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Asma</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Prostaglandine</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Prostaglandin</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Prostaglandina</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Voie respiratoire</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Respiratory tract</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Vía respiratoria</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Muscle lisse</s0><s5>13</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Smooth muscle</s0><s5>13</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Músculo liso</s0><s5>13</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2><s5>14</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2><s5>14</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2><s5>14</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Cobaye</s0><s5>54</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Guinea pig</s0><s5>54</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Cobayo</s0><s5>54</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Appareil respiratoire</s0><s5>57</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Respiratory system</s0><s5>57</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Aparato respiratorio</s0><s5>57</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Gustation</s0><s5>20</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Gustation</s0><s5>20</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Gusto</s0><s5>20</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Système gustatif</s0><s5>21</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Gustative system</s0><s5>21</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Sistema gustativo</s0><s5>21</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0><s5>22</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Respiratory disease</s0><s5>22</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0><s5>22</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Bronchopneumopathie obstructive</s0><s5>23</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Obstructive pulmonary disease</s0><s5>23</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad pulmonar obstructiva</s0><s5>23</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Dérivé de l'acide arachidonique</s0><s5>24</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Arachidonic acid derivatives</s0><s5>24</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Araquidónico ácido derivado</s0><s5>24</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Eicosanoïde</s0><s5>25</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Eicosanoid</s0><s5>25</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Eicosanoide</s0><s5>25</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Pathologie des bronches</s0><s5>26</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Bronchus disease</s0><s5>26</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Bronquio patología</s0><s5>26</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Pathologie des poumons</s0><s5>27</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Lung disease</s0><s5>27</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Pulmón patología</s0><s5>27</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fN21><s1>070</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 13-0101069 INIST</NO><ET>The bitter taste receptor (TAS2R) agonists denatonium and chloroquine display distinct patterns of relaxation of the guinea pig trachea</ET><AU>PULKKINEN (Ville); MANSON (Martijn L.); SAFHOLM (Jesper); ADNER (Mikael); DAHLEN (Sven-Erik)</AU><AF>The Unit for Asthma and Allergy Research, the National Institute of Environmental Medicine and the Centre for Allergy Research, Karolinska Institutet/Stockholm/Suède (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.); Research Programs Unit, Department of Medical Genetics, University of Helsinki/Finlande (1 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>American journal of physiology. Lung cellular and molecular physiology; ISSN 1040-0605; Coden APLPE7; Etats-Unis; Da. 2012; Vol. 47; No. 6; L956-L966; Bibl. 28 ref.</SO><LA>Anglais</LA><EA>Activation of taste receptors (TAS2Rs) by bitter taste agonists has been reported to cause bronchodilation. The aim of this study was to extend the information on the effects of bitter taste agonists on responses induced by different contractile mediators in a standard airway physiology preparation. Isometric responses were assessed in guinea pig trachea (GPT). TAS2R agonists were administered either to segments precontracted with different agonists for contraction or given before challenge with the different contractile stimuli, including antigen in tissues from ovalbumin-sensitized animals. TAS2R mRNA expression on GPT epithelium and smooth muscle was measured with real-time PCR. Denatonium, chloroquine, thiamine, and noscapine induced concentration-dependent relaxations (R<sub>max</sub>: 98.3 ± 1.6, 100.0 ± 0.0, 100.0 ± 0.0, and 52.3 ± 1.1% of maximum, respectively, in the presence of indomethacin) in segments precontracted with carbachol. The receptors for denatonium (TAS2R4, TAS2R10) and chloroquine (TAS2R3, TAS2R10) were expressed in GPT. Whereas denatonium selectively inhibited contractions induced by carbachol, chloroquine uniformly inhibited contractions evoked by prostaglandin E<sub>2</sub>, the thromboxane receptor agonist U-46619, leukotriene D<sub>4</sub>, histamine, and antigen. The effects of denatonium, but not those of chloroquine, were partly inhibited by blockers of the large Ca<sup>2+</sup>-activated K<sup>+</sup> channels and decreased by an increase of the level of precontraction. In conclusion, TAS2R agonists mediated strong relaxations and substantial inhibition of contractions in GPT. Chloroquine and denatonium had distinct patterns of activity, indicating different signaling mechanisms. The findings reinforce the hypothesis that TAS2Rs are potential targets for the development of a new class of more efficacious agonists for bronchodilation.</EA><CC>002A20; 002B11B</CC><FD>Saveur; Récepteur biologique; Agoniste; Chloroquine; Relaxation; Trachée; Bronchodilatation; Asthme; Prostaglandine; Voie respiratoire; Muscle lisse; Mammalia; Cobaye; Appareil respiratoire</FD><FG>Vertebrata; Gustation; Système gustatif; Pathologie de l'appareil respiratoire; Bronchopneumopathie obstructive; Dérivé de l'acide arachidonique; Eicosanoïde; Pathologie des bronches; Pathologie des poumons; Rodentia</FG><ED>Taste; Biological receptor; Agonist; Chloroquine; Relaxation; Trachea; Bronchodilation; Asthma; Prostaglandin; Respiratory tract; Smooth muscle; Mammalia; Guinea pig; Respiratory system</ED><EG>Vertebrata; Gustation; Gustative system; Respiratory disease; Obstructive pulmonary disease; Arachidonic acid derivatives; Eicosanoid; Bronchus disease; Lung disease; Rodentia</EG><SD>Sabor; Receptor biológico; Agonista; Cloroquina; Relajación; Tráquea; Broncodilatación; Asma; Prostaglandina; Vía respiratoria; Músculo liso; Mammalia; Cobayo; Aparato respiratorio</SD><LO>INIST-22200.354000182550680030</LO><ID>13-0101069</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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