The Amazonian oscar is extremely resistant to hypoxia, and tolerance scales with size. Overall ionoregulatory responses of small (~15 g) and large oscars (~200 g) to hypoxia were qualitatively similar, but the latter were more effective. Large oscars exhibited a rapid reduction in unidirectional Na⁺ uptake rate at the gills during acute hypoxia (PO₂ ~ 10 mm Hg) which intensified with time (7-8 h); Na⁺ efflux rates were also reduced, so net balance was little affected. The inhibitions were virtually immediate (1^st hour) and preceded a later 60 % reduction (at 3 h) in gill Na⁺,K⁺-ATPase activity, reflected in a 60% reduction in maximum Na⁺ uptake capacity without change in affinity (Km) for Na⁺. Upon acute restoration of normoxia, recovery of Na⁺ uptake was delayed for 1 h. These data suggest that dual mechanisms may be involved (e.g. immediate effects of O₂ availability on transporters, channels or permeability, slower effects of Na⁺K⁺ATPase regulation). Ammonia excretion appeared to be linked indirectly to Na⁺ uptake, exhibiting a Michaelis-Menten relationship with external [Na⁺], but the Km was less than for Na⁺ uptake. During hypoxia, ammonia excretion fell in a similar manner to Na⁺ fluxes, with a delayed recovery upon normoxia restoration, but the relationship with [Na⁺] was blocked. Reductions in ammonia excretion were greater than in urea excretion. Plasma ammonia rose moderately over 3 h hypoxia, suggesting that inhibition of excretion was greater than inhibition of ammonia production. Overall, the oscar maintains excellent homeostasis of ionoregulation and N-balance during severe hypoxia.