Ra. Pauwels et Gf. Joos, CHARACTERIZATION OF THE ADENOSINE RECEPTORS IN THE AIRWAYS, Archives internationales de pharmacodynamie et de therapie, 329(1), 1995, pp. 151-160
Adenosine causes bronchoconstriction both in vivo and in vitro in huma
n asthmatics. In an in vivo rat model of adenosine-induced bronchocons
triction, the order of bronchoconstrictor potency of adenosine analogu
es 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 ad
enosine receptors. The complete lack of bronchoconstrictory activity o
f CGS21680 suggests, nevertheless, that the A(2A) receptor subtype is
not involved in the adenosine-induced bronchoconstriction. A remarkabl
e finding was the dose-response curve to APNEA, which is thought to ha
ve some selective activity on the A(3) receptor. The A(2A)-selective a
ntagonist KF17837 (10(-7) to 10(-5) mol/kg) had no significant inhibit
ory activity on the adenosine-induced bronchoconstriction. The A(1) an
tagonists, KF15372 and KW3902, both significantly inhibited the NECA-i
nduced bronchoconstriction in BDE rats. We, therefore, conclude that t
he adenosine-induced bronchoconstriction in the rat is most likely due
to binding of adenosine to different receptor subtypes including the
A(1), A(2B) and A(3) subtypes.