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Cells of the outflow pathway respond to intraocular pressure increases by initiating homeostatic changes in the outflow resistance. Most of the studies have used sustained pressure, sensed as continuous mechanical stretching. However, trabecular meshwork cells are also exposed to cyclic mechanical stress relating to the ocular pulse. In a recent paper, Ramos et al. (1021)study the effects of cyclic mechanical stress on fluid flow across a monolayer of cell in culture.
It is important to assess the effects of cyclic mechanical stress in situ in the intact outflow pathway
Cyclic pressure oscillation causes decreased transcellular hydraulic conductivity, which is blocked by the Rho kinase inhibitor, Y27632, which affects cell cytoskeletal contractility. This suggests that Rho kinases modulated trabecular meshwork cell contractility is the key to the ability of the ocular pulse to affect hydraulic conductivity. The outcome of this study suggests that it will be important to assess the effects of cyclic mechanical stress in situ in the intact outflow pathway. These careful and well-designed studies have clear implications on the regulation of the outflow resistance and help explain how the ocular pulse affects aqueous humor outflow.