In fresh water fishes, ammonia is excreted across the branchial epithelium via passive NH(3) diffusion. This NH(3) is subsequently trapped as NH(4)(+) in an acidic unstirred boundary layer lying next to the gill, which maintains the blood-to-gill water NH(3) partial pressure gradient. Whole animal, in situ, ultrastructural and molecular approaches suggest that boundary layer acidification results from the hydration of CO(2) in the expired gill water, and to a lesser extent H(+) excretion mediated by apical H(+)-ATPases. Boundary layer acidification is insignificant in highly buffered sea water, where ammonia excretion proceeds via NH(3) diffusion, as well as passive NH(4)(+) diffusion due to the greater ionic permeability of marine fish gills. Although Na(+)/H(+) exchangers (NHE) have been isolated in marine fish gills, possible Na(+)/NH(4)(+) exchange via these proteins awaits evaluation using modern electrophysiological and molecular techniques. Although urea excretion (J(Urea)) was thought to be via passive diffusion, it is now clear that branchial urea handling requires specialized urea transporters. Four urea transporters have been cloned in fishes, including the shark kidney urea transporter (shUT), which is a facilitated urea transporter similar to the mammalian renal UT-A2 transporter. Another urea transporter, characterized but not yet cloned, is the basolateral, Na(+) dependent urea antiporter of the dogfish gill, which is essential for urea retention in ureosmotic elasmobranchs. In ureotelic teleosts such as the Lake Magadi tilapia and the gulf toadfish, the cloned mtUT and tUT are facilitated urea transporters involved in J(Urea). A basolateral urea transporter recently cloned from the gill of the Japanese eel (eUT) may actually be important for urea retention during salt water acclimation. A multi-faceted approach, incorporating whole animal, histological, biochemical, pharmacological, and molecular techniques is required to learn more about the location, mechanism of action, and functional significance of urea transporters in fishes.

Atlantic salmon (Salmo salar) were acclimated and exhaustively exercised at 12, 18, or 23°C to determine how temperature influences the magnitude of postexercise physiological disturbances. At each temperature, exercise led to decreased white muscle ATP and phosphocreatine concentrations. Phosphocreatine was rapidly restored within 1 h at each temperature whereas ATP restoration took 1-4 h at 18 and 23°C, but considerably longer at 12°C. Exercise-induced depletions of white muscle glycogen were accompanied by elevations in muscle lactate, which contributed to 0.6 unit decreases in white muscle intracellular pH (pHi) at each temperature. Compared with rates of recovery in warmer water, glycogen resynthesis, lactate catabolism, and pHicorrection were slower at 12°C. White muscle REDOX state estimates suggested that slower postexercise recovery at 12°C was not due to oxygen delivery limitations. Marked postexercise elevations in plasma osmolality and lactate concentration were also observed and in each case correction of the disturbance took longer at 12°C. Paradoxically, significant mortality (30%) was observed only at 23°C. We conclude that while warmer water facilitates postexercise recovery of white muscle metabolic and acid-base status in Atlantic salmon, extremely high temperatures may make them more vulnerable to delayed postexercise mortality.

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