Figure12. cGMP-assisted modification of IOP via increase in aqueous humour (AqH) outflow.(a) Nitric oxideactivates generation of cGMP by GC-1. The cGMP activates protein kinase G (PKG). The PKG so activated can phosphorylate numerous targets with various downstream effects, including inhibition of Ras homolog family member A (RhoA).This prevents inhibition of myosin phosphatase by Rho Kinase. (b) Besides inhibition of RhoA, activated PKG can directly trigger myosin light chain phosphatase (MLCP). Thereafter, dephosphorylation of the regulatory light chain of myosin by MLCP prevents actin–myosin interaction, promoting cell relaxation. (c) This, then leads to a widening of the intercellular spaces in the juxtacanalicular trabecular meshwork (TM) and Schlemm’s canal.This facilitates conventional AqH outflow and thereby lowering IOP.