Meeting Abstract

83.3  Tuesday, Jan. 6 10:45  Acid-base compensation in marine fish gill during osmoregulation YAO, Z.*; GROSELL, M.; HEUER, R.M.; RUHR, I.; SCHAUER, K.; RSMAS, University of Miami；East China Sea Fisheries Research Institute,CAFS; RSMAS, University of Miami; RSMAS, University of Miami; RSMAS, University of Miami; RSMAS, University of Miami zyao@rsmas.miami.edu

It is well known that marine fish must drink seawater to compensate for continual water loss caused by their dehydrating environment. Intestinal water absorption is linked to substantial intestinal base excretion. Previous research has shown that fish transferred to hypersalinity experience a perturbation in acid-base balance. The gill may play an important role in compensating for the increased intestinal base loss that occurs during hypersalinity exposure. To test this hypothesis, Gulf toadfish were exposed to hypersalinity (60ppt), which is known to increase intestinal HCO₃^– excretion. Exposure to 60ppt seawater resulted in an immediate metabolic acidosis with a significant decrease in blood pH and HCO₃^–, followed by a recovery of blood pH by a decrease in pCO₂ and an increase in HCO₃^–. A similar metabolic acidosis and recovery were found when fish were exposed to 60ppt HCO₃^– free seawater (HEPES buffered). These results suggest that compensation for intestinal base loss during hypersalinity is from gill H⁺ excretion rather than from gill HCO₃^– uptake from seawater. This increased H⁺ excretion may be regulated by relocation of the V-H⁺-ATPase and/or increased abundance of NHE2 and/or NHE3. The immunolocalization of V-H⁺-ATPase as well as, gene expression of NHE2 and NHE3 in the branchial epithelium is currently being investigated.