Acid-base regulation in rainbow trout acclimated to about 3, 100 and 500 mmol l−1 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 PCOCO2 to about 1.15kPa (8.5mmHg, 3mmol l−1), 1.33kPa (10mmHg, 100 mmol l−1) or 1.5 kPa (11.2 mmHg, 500 mmol l−1) 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 300 mmol l−1 Na+ and Cl−, respectively. [HCO3−] in animals acclimated to 100 and 500 mmol l−1 rose to higher values than that in fish at 3 mmol l−1.
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, [Tamm], 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 300 mmol l−1 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−/Cl− exchange processes for the compensation of extracellular pH during respiratory acidoses in fish.