Revisiting the usefulness of @entity2404 modulation in the treatment of bronchoconstriction in XXXX .

@entity1 @entity748 @entity2404 @entity565 @entity2918 @entity141
UNASSIGNED: Airway smooth muscle (ASM) is the effector cell in the bronchoconstrictory pathway. It is believed that the bronchoconstriction present in @entity565 is associated with changes in the airway milieu that affect ASM excitation-contraction coupling and @entity141 -handling. Asthmatics also react differently to ventilatory mechanical strain. Deep inspiration (DI), which produces bronchodilation in healthy individuals, is less effective in @entity748 , and even enhances bronchoconstriction in moderate to severely affected @entity1 . Our laboratory has previously studied the mechanotransductory pathway of airway stretch-activated contractions (Rstretch) leading to DI-induced bronchoconstriction. We demonstrated the ability of agonists acting through @entity2404 (TxA2) receptors to amplify airway Rstretch responses. Despite the involvement of excitatory @entity2918 in bronchoconstriction, clinical trials on treatments targeting TxA2-synthase inhibition and TP-receptor antagonism have produced mixed results. Studies in Western populations produced mostly negative results, whereas studies performed in Asian populations showed mostly positive outcomes. In this review, we discuss the role of TxA2-synthase inhibition and TP-receptor antagonism in the treatment of @entity748 . We present information regarding variations in study designs and the possible role of TP-receptor gene polymorphisms in previous study outcome discrepancies. Perhaps future studies should focus on @entity748 @entity1 with DI-induced bronchoconstriction in particular, planting the seed for the individualized treatments for @entity748 .
