Smooth muscle contraction can be divided into two phases: the initial contraction determines the amount of developed force and the second phase determines how well the force is maintained. The initial phase is primarily due to activation of actomyosin interaction and is relatively well understood, whereas the second phase remains poorly understood. Force maintenance in the sustained phase can be disrupted by strains applied to the muscle; the strain causes actomyosin cross-bridges to detach and also the cytoskeletal structure to disassemble in a process known as fluidization, for which the underlying mechanism is largely unknown. In the present study we investigated the ability of airway smooth muscle to maintain force after the initial phase of contraction. Specifically, we examined the roles of Rho-kinase and @entity7131 ( @entity7131 ) in force maintenance. We found that for the same degree of initial force inhibition, Rho-kinase substantially reduced the muscle's ability to sustain force under static conditions, whereas inhibition of @entity7131 had a minimal effect on sustaining force. Under oscillatory strain, Rho-kinase inhibition caused further decline in force, but again, @entity7131 inhibition had a minimal effect. We also found that Rho-kinase inhibition led to a decrease in the @entity3999 filament mass in the muscle cells, suggesting that one of the functions of Rho-kinase is to stabilize @entity3999 filaments. The results also suggest that dissolution of @entity3999 filaments may be one of the mechanisms underlying the phenomenon of fluidization. These findings can shed light on the mechanism underlying deep inspiration induced bronchodilation.

Force maintenance and XXXX filament assembly regulated by Rho-kinase in airway smooth muscle.

@entity3999 :: ('79784', 'Gene') :: ['myosin'] @entity7131 :: ('MESH:D020151', 'Disease') :: ['protein kinase C', 'PKC']
@entity3999 :: (79784,Gene) :: ['myosin']
