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Dellabianca, Antonio; Faniglione, Marisa; De Angelis, Stefano; Tonini, Stefano; Balestra, Barbara; Colucci, Mario; Cervio, Marila; Clavenzani, Paolo; Chiocchetti, Roberto; De Giorgio, Roberto; Candura, Stefano M.

Adenosine A1 and A3 Receptor Agonists Inhibit Nonadrenergic, Noncholinergic Relaxations in the Guinea Pig Isolated Trachea

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  • Media type: E-Article
  • Title: Adenosine A1 and A3 Receptor Agonists Inhibit Nonadrenergic, Noncholinergic Relaxations in the Guinea Pig Isolated Trachea
  • Contributor: Dellabianca, Antonio; Faniglione, Marisa; De Angelis, Stefano; Tonini, Stefano; Balestra, Barbara; Colucci, Mario; Cervio, Marila; Clavenzani, Paolo; Chiocchetti, Roberto; De Giorgio, Roberto; Candura, Stefano M.
  • Published: S. Karger AG, 2009
  • Published in: Respiration, 78 (2009) 1, Seite 75-83
  • Language: English
  • DOI: 10.1159/000183755
  • ISSN: 0025-7931; 1423-0356
  • Origination:
  • Footnote:
  • Description: <i>Background:</i> Adenosine affects the tone and reactivity of airways by activating specific membrane receptors, named A<sub>1</sub>, A<sub>2a</sub>, A<sub>2b</sub> and A<sub>3</sub>. It affects cellular activities either directly by regulating membrane ion exchanges and polarization, or indirectly by modifying neurotransmitter release. <i>Objectives:</i> We assessed the effect of A<sub>1</sub> and A<sub>3</sub> receptor activation on electrically induced nonadrenergic, noncholinergic (NANC) relaxations in the guinea pig isolated trachea and the localization of A<sub>1</sub> and A<sub>3</sub> receptors in tracheal inhibitory neurons. <i>Methods:</i> NANC responses at 3 Hz were evaluat- ed in the presence of 2-chloro-N<sup>6</sup>-cyclopentyladenosine (CCPA), a selective A<sub>1</sub> agonist, and 2-chloro-N<sup>6</sup>-(3-iodobenzyl)-adenosine-5′-N-methyluronamide (Cl-IB-MECA), a selective A<sub>3</sub> agonist, before and after the administration of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective A<sub>1</sub> antagonist, or 9-chloro-2-(2-furanyl)-5-((phenylacetyl)amino[1,2,4]triazolo[1,5-c])quinazoline (MRS 1220), a selective A<sub>3</sub> antagonist, respectively. For immunohistochemistry, tissues were exposed to antibodies to HuC/D, a general neuronal marker, neuronal nitric oxide synthase (nNOS), and A<sub>1</sub> or A<sub>3</sub> adenosine receptors and processed by indirect immunofluorescence. <i>Results:</i> CCPA (10 n<i>M</i>–3 μ<i>M</i>) inhibited NANC relaxations. DPCPX (10 n<i>M</i>) failed to antagonize the effect of CCPA, but inhibited per se NANC relaxations (range 0.1–100 n<i>M</i>). CCPA (10 n<i>M</i>–10 μ<i>M</i>) contracted unstimulated tracheal preparations, an effect antagonized by 10 n<i>M</i> DPCPX, with a pK<sub>B</sub> value of 8.43. Cl-IB-MECA (10 n<i>M</i>–3 μ<i>M</i>) inhibited NANC relaxations through a mechanism antagonized by MRS 1220 (100 n<i>M</i>). A<sub>1</sub>- and A<sub>3</sub>-positive neurons containing nNOS were detected in tracheal sections. <i>Conclusions:</i> Enogenous adenosine may induce airway hyperresponsiveness by inhibiting NANC relaxations via A<sub>1</sub> and A<sub>3</sub> receptors.