| Research Abstract |
1. When bronchial smooth muscle contracted by ACh in normal rats, a monomeric GTP binding protein, RhoA, translocated to plasma membrane (RhoA activation). The bronchial muscle from repeatedly antigen-challenged rats more markedly contracted by ACh, and the RhoA activation was also more markedly augmented in the muscle. These suggest that augmentation of RhoA activation may be a crucial factor in airway hyperresponsiveness at allergic bronchial asthma.
2. In β-escin-penneabilized intrapulmonary bronchial smooth muscle, ACh induced a further contraction under the same [Ca^<2+>]_i, i.e. Ca^<2+> sensitization. Rho kinase (ROCK) inhibitor, Y-27632, completely blocked the Ca^<2+> sensitization, suggesting that RhoA/ROCK-mediated Ca^<2+> sensitization may be involved in the airway hyperesponsiveness.
3. An augmentation of ACh-induced contraction of antigen-challenged bronchial smooth muscle was obviously observed, but that of tracheal smooth muscle was not. This correlated the fact that RhoA expression in bronchial, but not tracheal, smooth muscle was significantly increased in the antigen-treated rats. This suggests that the increased expression of RhoA has an important role in developing hyperesponsiveness of bronchial smooth muscle.
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