The concept of the conventional aqueous outflow pathway (through the trabecular meshwork and other components of the canal's inner wall, along Schlemm's canal to collector channels, and out of the eye through the collector channels) was modeled on tubes with leaky walls and a network of electrical resistances. Analysis of these models suggested experiments to test the models and to assess the magnitude of the resistance of portions of the pathway. We found that the well-known increase in outflow resistance with increased intraocular pressure was, in large measure, the result of blockage of the collector channels, probably by the canal's inner wall. A model of the trabecular meshwork predicted that tension on the scleral spur and trabecular mesh would cause the meshwork to arch over Schlemm's canal. We depressed the lens to generate such tension, and found that the resistance of the inner wall of the canal decreased. In one eye, lens depression also decreased resistance to flow in the collector channels and the canal of Schlemm and prompted the suggestion that when secretory inhibitors are used in glaucoma, cyclo-tonic agents should be used simultaneously to relieve canal collapse and blockage of collector channels by inner canal wall.