Recent studies have suggested that the bladder urothelium is sensitive to both stretch and hydrostatic pressure during bladder filling, and is considered to play a mechanosensory role in sensing bladder fullness [1, 2]. In a previous study [3], our group demonstrated that compared to the control, rat bladder urothelial cells (UCs) exposed to hydrostatic pressure (10–15 cmH2O for 5 minutes) in vitro released significantly higher levels of ATP and that this response was attenuated by pharmacologically blocking transient receptor potential (TRP) channels, as well as epithelial sodium channels (ENACs). While blocking these ion channels inhibited the ATP response by UCs to hydrostatic pressure, it remains unclear whether these ion channels are being activated directly by hydrostatic pressure or by membrane deformation. Our current hypothesis is that a change in cell volume may occur due to the application of hydrostatic pressure and subsequent changes in cellular osmolality, which, in turn, activate the membrane-bound mechanosensitive channels. Using real-time fluorescent imaging and a custom experimental setup, the present study sought to quantify the UC cell volume changes during exposure to hydrostatic pressure and to better understand the mechanisms by which UCs sense hydrostatic pressure.

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