Recent studies have demonstrated the involvement of intrapulmonary activation of the renin-angiotensin system (RAS) in the progression of various pulmonary diseases. We analyzed to what extent the pulmonary RAS could modulate the development of allergic lung disease. Therefore, valsartan (a blocker of angiotensin II type 1 receptors; 0.5 mM) or pepstatin A (a renin inhibitor; 0.5 mM) were nebulized during the last week of sensitization protocol. The bronchial reactivity, total number of cells from bronchoalveolar lavage fluid (BALF) and inflammatory cell infiltration were assessed. Valsartan treatment reduced allergen - induced bronchoconstriction by more than 20%, and (within 1300 characters including spaces, decreased Emax of contraction induced by acetylcholine (ACh) (with 16.86%). Both, valsartan and pepstatin A, prevented the challenge-induced alteration of the bronchorelaxant effect of terbutaline and decreased the total number of cells from BALF. Even more, valsartan treatment decreased infiltration of inflammatory cells on the walls of lobar and segmental bronchi and in peribronchiolar space from this level. These results emphasize the RAS roles on such pathophysiological circumstances and suggest that blocking of pulmonary RAS could partially prevent the effects of allergen sensitization/ challenge.

Keywords: 

airway, allergy, angiotensin