Effect of Environmental Water Salinity on Acid-base Regulation during Environmental Hypercapnia in the Rainbow Trout (oncorhynchus Mykiss)

Acid-base regulation in rainbow trout acclimated to about 3, 100 and SOOmmolP Na and Cl~, at constant water [HCO3~], was assessed during 24h of exposure to 1 % CO2 and during recovery. The respiratory acidosis induced by a rise in plasma Pco2 to about 1.15kPa (8.5mmHg, Smmoll" ), 1.33kPa (lOmmHg, lOOmmoir) or 1.5 kPa (11.2 mmHg, SOOmmoll") was partially compensated for by accumulation of plasma HCO3~. The degree of pH compensation depended on the salinity of the environmental water, being about 61,82 and 88% at 3, 100 and SOOmmoll" Na and Cl~, respectively. [HCO3~] in animals acclimated to 100 and SOOmmoll" rose to higher values than that in fish at 3mmoll~'. Plasma [Cl~] decreased during hypercapnia as compared to control concentrations in all groups of fish. Plasma [Na] rose during the first 8 h of hypercapnia in fish acclimated to all three salinities, but recovered towards control values during the remainder of hypercapnia. The rise in plasma [HCO3~] was significantly related to the fall in plasma [Cl~], whereas the changes in plasma [Na] were unaffected by simultaneous changes in plasma [HCO3~]. Time courses of changes in plasma [Na] and total ammonia concentration, [ r a m m ] , were similar but in opposite directions. The transepithelial potential (TEP) of blood relative to water was negative, close to zero and positive, averaging —21, —5.8 and +6.2 mV for fish acclimated to 3, 100 and 300mmolP' Na, respectively. After initiation of hypercapnia, which caused a quite heterogeneous response among groups, a clear trend towards depolarization was observed during the remainder of hypercapnia. These results confirm the role of active HCO3"/C1~ exchange processes for the compensation of extracellular pH during respiratory acidoses in fish.