The interactions of acid-base status, waste nitrogen excretion and metabolism in the gulf toadfish Opsanus beta, a ureogenic teleost, were examined by exposing toadfish to a variety of water treatments. Our measurements show that, like other marine teleosts, toadfish rapidly regulate acid- base status by manipulating blood [HCO3-]. Several treatments affected nitrogen excretion. The initial stages of hypercapnia (1 % CO2) led to significant reductions in ureogenesis, and the later compensated stages (with elevated plasma [HCO3-]) led to significant increases in ureogenesis. Treatment of water with HCl (which lowered pH and reduced the carbonate content) substantially inhibited ureogenesis. Subsequent experiments with NH4Cl loading and several other treatments suggest that this depression is less likely to be the result of acid-base perturbations, but is probably an enhancement of the fish's ability to excrete waste nitrogen as ammonia, thereby decreasing the drive for ureogenesis. Enzyme activities and hepatocyte ureogenic potential were unaffected by various acid-base treatments, but a significant depletion of plasma amino acid levels was associated with the increase in plasma [HCO3-] induced by hypercapnia. Changes in ureogenesis associated with our treatments appear to be due primarily to changes in substrate levels, rather than to wholesale changes of the biochemical machinery. Our results are discussed in the context of the hypothesis of Atkinson and colleagues, that ureogenesis is a means for acid-base regulation via bicarbonate consumption.

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