Figure 3: Regulation of IOP by different classes of molecules and mediators. (a) Central role of cAMP in the regulation of neat AH production. A decrease of cAMP in NPE ciliary cells appears to lead to a decreased efflux through the ATP-dependent Na+/K+ channel; an increase of ATP might trigger the activation of the chloride maxi channel in PE ciliary cells, leading to “inverse secretion” towards the stroma, finally reducing the AH influx into the anterior chamber. CA inhibitors work independently of cAMP and decrease carbonate exchange with the stroma, finally reducing chloride transit to the anterior chamber and water secretion. GJ: gap junctions; TJ: tight junctions; MT1,2,3: melatonin receptors; CA: carbonic anhydrase. (b) An increase of cAMP induced by forskolin or melatonin through the MT3 receptors may lead to inhibition of the Rho kinase, which in turn results in the disorganization of the TM cells cytoskeleton and finally to an increased TM outflow. (c) Prostaglandin analogs upregulate MMPs (matrix metalloproteases) which degrade extracellular proteins (mainly collagen) in the uveoscleral pathway, thus increasing AH outflow through this way.