Nitrogenous Waste Excretion, Acid-Base Regulation, and lonoregulation in Rainbow Trout (<i>Oncorhynchus mykiss</i>) Exposed to Extremely Alkaline Water

Abstract

Rainbow trout (Oncorhynchus mykiss) survived in alkaline fresh water (pH = 9.50) for 72 h, although the exposure rendered the fish more susceptible to mortality from other causes. At pH 9.50 ammonia excretion (JAmm) was initially blocked, and total plasma ammonia levels increased. However, JAmm steadily recovered thereafter; by 48 h control rates were reestablished and plasma total ammonia stabilized at six times the control level. The initial blockade of JAmm was associated with a reversal of the blood to bulk water PNH₃ gradient. Paradoxically, the continued depression of JAmm until 48 h occurred despite the presence of favorable blood-to-water gradients for passive NH₃ and $$NH_{4}^{+}$$ difusion. An increase in urea excretion helped sustain waste N excretion in the face of inhibited JAmm. A respiratory alkalosis (decreased arterial Pco₂, increased arterial pH) occurred initially but was partially counteracted by a metabolic acidosis (decreased plasma $$HCO_{3}^{-}$$), which stabilized arterial pH at about 8 0 throughout the exposure. Increases in blood lactate, without marked changes in arterial O₂ tension, suggested that an activation of glycolysis occurred that was not caused by hypoxemia. Plasma Na⁺ and Cl⁻ levels decreased by about 7% during the first 24 h of exposure but stabilized thereafter.