An animal model for adenosine-induced bronchoconstriction.
The inhalation of adenosine is known to cause bronchoconstriction in asthmatic patients. A thorough study of the possible role of this purine nucleoside in the pathogenesis of asthma has been hampered by the lack of a suitable animal model. We have studied the bronchial effects of adenosine in an in vivo rat model. The intravenous injection of 0.1 to 10 micromoles/kg body weight of adenosine causes in BDE-rats an increase in lung resistance and decrease in dynamic compliance. Study of the potency of various adenosine analogs suggests that the bronchial adenosine receptor belongs to the A2-type. The bronchoconstriction caused by adenosine is inhibited by atropine, methysergide, sodium cromoglycate, nedocromil sodium, and ketotifen. Xanthines in doses of 5 and 15 mg/kg body weight have no significant effect on the adenosine-induced bronchoconstriction. These results suggest that adenosine causes bronchoconstriction by stimulating postsynaptic vagal nerve endings and mast cells.
D000241:Adenosine / Q000494:pharmacology*; D000403:Airway Resistance / Q000187:drug effects; D000818:Animals; D001696:Biomechanical Phenomena; D001980:Bronchi / Q000378:metabolism; D001986:Bronchial Spasm / Q000139:chemically induced* / Q000188:drug therapy / Q000503:physiopathology; D004195:Disease Models, Animal; D008170:Lung Compliance / Q000187:drug effects; D051381:Rats; D011983:Receptors, Purinergic / Q000378:metabolism; D014970:Xanthines / Q000627:therapeutic use
D011983:Receptors, Purinergic; D014970:Xanthines; D000241:Adenosine