Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for two weeks to freshwater (1 ‰ salinity), brackish water (11 ‰) or full strength seawater (35 ‰) under normoxic conditions (water Po2 = 158 mmHg) and then subjected to 48 h of continued normoxia or hypoxia at a level (Po2 = 54 mmHg) close to but above the critical Po2. Plasma osmolality, [Na+] and [Cl-] increased with increasing salinity, but the rises were limited, reflecting an effective extracellular osmoregulation. Muscle water content was the same at all three salinities, indicating complete cell volume regulation. Gill Na+/K+-ATPase activity did not change with salinity, but hypoxia caused a 25 % decrease in branchial Na+/K+-ATPase activity at all three salinities. Furthermore, hypoxia induced a significant decrease in mRNA levels of the Na+/K+-ATPase α1-subunit, signifying a reduced expression of the transporter gene. The reduced ATPase activity did not influence extracellular ionic concentrations. Blood [Hb] was stable with salinity, and it was not increased by hypoxia. Instead, hypoxia decreased the erythrocytic nucleoside triphosphate content, a common mechanism for increasing blood O2 affinity. It is concluded that moderate hypoxia induced an energy saving decrease in branchial Na+/K+-ATPase activity, which did not compromise extracellular osmoregulation.
Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology, 2008, Vol 178, p. 909-915