Ionic regulation and nitrogenous excretion in rainbow trout exposed to buffered and unbuffered freshwater of pH 10.5.

Rainbow trout exposed to unbuffered water of pH 10.5 initially showed significant increases in blood pH, plasma cortisol and glucose, partial pressure of NH3 (PNH3), NH4+, and HCO3- values as well as loss of plasma Cl-, reduced partial pressure of CO2 (PCO2), and inhibition of total ammonia excretion rate. After the first day, fish resisted further change, and new levels were established (for blood pH and plasma PCO2 and PNH3 levels) or imbalances corrected, either partially (for total ammonia excretion) or completely (for plasma Cl-, HCO3-, cortisol, and glucose values). During the 7-d exposure, 80% of fish in unbuffered water survived, but in buffered water (0.75 mmol L(-1) glycine-buffered KOH at pH 10.5), survival was only 50% after 3 d, and ion regulatory failure was evident. Fish in buffered and unbuffered alkaline waters had similar total ammonia excretion rates, which suggests that glycine-buffered KOH was not sufficient to significantly reduce gill boundary layer acidification. After 7 d in unbuffered alkaline water, 30% of total ammonia excretion was linked with an amiloride-sensitive (0.1 mmol L(-1)) Na+ uptake mechanism. Treatment of alkaline-exposed trout with waterborne acetazolamide (1.5 mmol L(-1)) indicated that gill boundary layer H+ production, through hydration of CO2, had a role in excretion of total ammonia. Exposure to 4-acetamino-4'-isothiocyantostilbene-2,2'-disulphonic acid (SITS; 0.1 mmol L(-1)) following 24-h exposure to unbuffered alkaline water resulted in increased plasma HCO3- and lowered plasma Cl- concentrations, indicating the role of branchial Cl-/HCO3- exchange in regaining Cl- lost and eliminating the HCO3- accumulated during exposure to alkaline water.