Adenosine is an endogenously purine nucleoside which plays a significant role in regulation of airways tone and reactivity by multiple and incompletely known mechanisms, including the release of endogenously active peptides from mast cells via activation of the A3 receptors. Our previous results suggested that releasing of enzymes from activated mast cells could activate the intrapulmonary renin angiotensin system (RAS). In this study, we investigated the involvement of angiotensin II (Ang II) in adenosine-induced bronchoconstriction in an experimental model of allergic asthma. On bronchial rings from ovalbumin (OVA) sensitized rats, after in vitro challenge, adenosine induced small contractile effects which became significant after indomethacin pre-treatment. On the other hand adenosine pre-treatment amplified bronchoconstriction induced by the allergen (OVA) challenge and reduced bronchial relaxation of acetylcholine pre-contracted bronchial rings by cumulative doses of terbutaline. All these effects are significantly lower on rats treated with losartan (a blocker of Ang II type 1 specific receptors, AT1) in the last two weeks of sensitization protocol (50 mg/kg/day). Our data confirmed that adenosine induced bronchial hyperreactivity could be partially a result of RAS activation in abnormal conditions as antigen sensitization and challenge.