The mechanism of the methacholine-induced rise in intraocular pressure in the dog was studied to determine the basis of the relationship, if any, between lens thickness and intraocular pressure. The results rule out a vasodilator component in methacholine intraocular pressure elevation, and the tonometric recording of the elevation makes unlikely the involvement of methacholine stimulation of the rectus muscles of the eye. Thus, indirect evidence points to methacholine stimulation of ciliary muscle contraction with consequent thickening of the lens as responsible for its intraocular pressure-elevating effect and, hence, the ability of the response under investigation to specify the cycloplegic liability of a neurotropic antispasmodic agent.
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