Ammonia is a toxic nitrogenous waste causing ionoregulatory and neuronal dysfunction in aquatic animals. Ammonotelic animals excrete ammonia as is and must have therefore an efficient excretion process in place to keep blood/hemolymph ammonia levels in a tolerable range. While in fish and crustaceans, the excretory mechanism has been investigated in greater detail, the cellular regulation of these processes is rather unknown. To investigate which cellular pathways are involved in ammonia excretion, gills from osmoregulating green crabs were perfused with a hemolymph-like solution containing 500µM NH4Cl, mimicking hemolymph levels found after feeding. Activation of the PKA pathway by adding either Forskolin or 8-Bromo-cAMP, which is known to activate osmoregulatory NaCl uptake in crustaceans, to the perfusion solution caused a significant decrease in the ammonia excretion rate. By contrast, activating the PKG pathway by the addition of 8-Bromo-cGMP, caused an increase of excretion, which was blocked when PKG activity was inhibited via KT5823. When no ammonia was added to either side of the branchial epithelium, metabolic ammonia was released predominantly to the environment. Interestingly, the addition of 8-Bromo-cAMP caused not only an increase of ammoniagenesis, it also promoted that a higher proportion of metabolic ammonia is released towards the hemolymph side, while apical release remained unaltered.