Michael P. Wilkie

Mechanisms of Ammonia Excretion Across Fish Gills

Although it has been a subject of considerable research, many questions regarding the mechanism(s) of ammonia excretion (JAmm) across fish gills remain unresolved. Recent advances improving our understanding of the linkage between CO2 and ammonia excretion, and the likelihood that H+-ATPases are present in freshwater fish gills, should improve our understanding about mechanisms of branchial JAmm. Moreover, basic differences in gill structure and function between freshwater- and seawater-adapted fishes are probably reflected by dissimilar mechanisms of JAmm. In fresh water, JAmm likely proceeds exclusively by NH3 diffusion down favorable blood-to-expired gill water PNH3 gradients. The carbonic anhydrase-catalyzed hydration of excreted CO2 augments JAmm by generating H+ that trap NH3 (as NH4+) as it diffuses into the gill water. To a lesser extent, the active extrusion of H+, via branchial H+-ATPases, might also facilitate JAmm. The probable absence of electroneutral Na+/H+ exchange on the apical epithelia, makes branchial Na+/NH4+ exchange unlikely in freshwater fishes. In marine fishes, JAmm likely occurs via passive NH3 diffusion but NH4+ diffusion is also important, owing to the much higher cationic permeability of the gills of seawater fishes. The high Na+ concentrations of seawater indicate that apical Na+/NH4+ exchange is also possible in marine fishes. Finally, substitution of NH4+ for K+ on basolateral Na+:K+ATPases and/or Na+/2Cl−/K+ co-transporters could also contribute to JAmm by marine fishes.

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

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

NaCl transport and ultrastructure of opercular epithelium from a freshwater-adapted euryhaline teleost, Fundulus heteroclitus

NH_{4}^{+}

Modes of metal toxicity and impaired branchial ionoregulation in rainbow trout exposed to mixtures of Pb and Cd in soft water.

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

Physiological adaptations of rainbow trout to chronically elevated water pH (pH = 9.5)

HCO_{3}^{-}

Influence of natural organic matter (NOM) quality on Cu-gill binding in the rainbow trout (Oncorhynchus mykiss).

), 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.