A marine teleost, Opsanus beta , compensates acidosis in hypersaline water by H + excretion or reduced HCO 3 − excretion rather than HCO 3 − uptake

Increases in ambient salinity demand parallel increases in intestinal base secretion for maintenance of osmoregulatory status, which is likely the cause of a transient acidosis following transfer of euryhaline fish from freshwater to seawater. It was predicted that transfer of the marine Gulf toadfish ( Opsanus beta ) from seawater (35 ppt) to hypersaline (60 ppt) seawater (HSW) would lead to a transient acidosis that would be compensated by increases in branchial acid excretion to offset the acid–base disturbance. Toadfish exposed to HSW showed a significant decrease in blood pH and [HCO 3 − ] but no increase in pCO 2 , followed by a full recovery after 48–96 h. A similar metabolic acidosis and recovery was found when fish were exposed to 60-ppt HCO 3 − -free seawater (HEPES-buffered), which may suggest that compensation for intestinal base loss during hypersaline treatment is from gill H + excretion rather than gill HCO 3 − uptake. However, we cannot rule out that reduced branchial HCO 3 − excretion contributed to an increase in net acid excretion. Since colchicine prevents full compensation, translocation of H + and/or HCO 3 − transporters between cytosolic compartments and plasma membrane fractions might be involved in compensating for the hypersalinity-induced acidosis. Translocation of transporters rather than de novo synthesis may represent a faster and less energetically demanding response to rapidly fluctuating and high salinities encountered by toadfish in their natural environment.