LAUSR

ABSTRACT Invertebrates employ a variety of ammonia excretion strategies to facilitate their survival in diverse aquatic environments, including freshwater, seawater and the water film surrounding soil particles. Various environmental properties set innate challenges for an organism's ammonia excretory capacity. These include the availability of NaCl and the respective ion-permeability of the organism's transport epithelia, and the buffering capacity of their immediate surrounding medium. To this end, some transporters seem to be conserved in the excretory process. This includes the Na+/K+(NH4+)-ATPase (NKA), the NH3/CO2 dual gas-channel Rhesus (Rh)-proteins and novel ammonia transporters (AMTs), which have been identified in several invertebrates but appear to be absent from vertebrates. In addition, recent evidence strongly suggests that the hyperpolarization-activated cyclic nucleotide-gated K+ channel (HCN) plays a significant role in ammonia excretion and is highly conserved throughout the animal kingdom. Furthermore, microtubule-dependent vesicular excretion pathways have been found in marine and soil-dwelling species, where, unlike freshwater systems, acid-trapping of excreted ammonia is difficult or absent owing to the high environmental buffering capacity of the surroundings. Finally, although ammonia is known to be a toxic nitrogenous waste product, certain marine species readily maintain potentially toxic hemolymph ammonia as a sort of ammonia homeostasis, which suggests that ammonia is involved in physiological processes and does not exist simply for excretion. Such findings are discussed within this Commentary and are hypothesized to be involved in acid–base regulation. We also describe excretory organs and processes that are dependent on environmental constraints and indicate gaps in the current knowledge in these topics. Summary: This Commentary discusses the ammonia excretion strategies of invertebrates inhabiting a variety of different aquatic environments as well as the roles of excretory proteins in acid–base homeostasis.