Aqueous outflow tissue deformation caused by normal intraocular pressure transients induces pulsatile one-way discharge of aqueous to the vascular system. The model identifies biomechanical coupling of intraocular pressure with aqueous outflow tissue deformation and also sites of high flow capable of inducing shear stress. These mechanotransduction mechanisms, well characterized as a means of controlling pressure and flow in the vascular system, also provide a means of regulatory feedback to control intraocular pressure and aqueous flow.
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Murray Johnstone (2004) studied this question.
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