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Arch Int Pharmacodyn Ther. 1995 Jan-Feb;329(1):151-60.

Characterization of the adenosine receptors in the airways.

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Department of Respiratory Diseases, University Hospital Ghent, Belgium.


Adenosine causes bronchoconstriction both in vivo and in vitro in human asthmatics. In an in vivo rat model of adenosine-induced bronchoconstriction, the order of bronchoconstrictor potency of adenosine analogues was NECA = CPA > APNEA > CHA > R-PIA > CGS21680. This order of potency does not fit with the classical order of potency for a single subtype of adenosine receptors. The complete lack of bronchoconstrictory activity of CGS21680 suggests, nevertheless, that the A2A receptor subtype is not involved in the adenosine-induced bronchoconstriction. A remarkable finding was the dose-response curve to APNEA, which is thought to have some selective activity on the A3 receptor. The A2A-selective antagonist KF17837 (10(-7) to 10(-5) mol/kg) had no significant inhibitory activity on the adenosine-induced bronchoconstriction. The A1 antagonists, KF15372 and KW3902, both significantly inhibited the NECA-induced bronchoconstriction in BDE rats. We, therefore, conclude that the adenosine-induced bronchoconstriction in the rat is most likely due to binding of adenosine to different receptor subtypes including the A1, A2B and A3 subtypes.

[Indexed for MEDLINE]

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