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 300mmoll⁻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 to about 1.15kPa (8.5mmHg, 3mmoll⁻¹), 1.33kPa (10 mmHg, 100 mmol I⁻¹) or 1.5 kPa (11.2 mmHg, 300 mmol I⁻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 300mmoll⁻¹ Na⁺ and Cl⁻, respectively. [HCO₃⁻] in animals acclimated to 100 and 300 mmol I⁻¹ rose to higher values than that in fish at 3 mmol I⁻¹.

Plasma [Cl⁻] decreased during hypercapnia as compared to control concentrations in all groups of fish. Plasma [Na⁺] rose during the first 8h 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, [T_amm], 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 I⁻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⁻/C1⁻ exchange processes for the compensation of extracellular pH during respiratory acidoses in fish.