Abstract
Carbon dioxide excreted across fish gills is hydrated catalytically to form HCO 3 − and H+ ions in water near the gill surface. We tested the possibility that CO2 excretion is functionally linked to ammonia excretion through chemical reactions in the gill-water boundary layer. A bloodperfused trout head preparation was utilized in which the convective and diffusive components of branchial gas transfer were controlled. Pre-incubation of blood perfusate with the carbonic anhydrase inhibitor, acetazolamide, reduced both carbon dioxide and ammonia excretion in the blood-perfused preparation. Increasing the buffering capacity of inspired ventilatory water significantly reduced ammonia excretion, but carbon dioxide excretion was unaffected. Each of these experimental treatments significantly reduced the acidification of ventilatory water flowing over the gills. It is proposed that the catalysed conversion of excreted CO2 to form HCO 3 − and H+ ions provides a continual supply of H+ ions need for the removal of NH3 as NH 4 + . We suggest, therefore, that acidification of boundary layer water by CO2 enhances blood-to-water NH3 diffusion gradients and facilitates ammonia excretion.
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Topics from this Paper
Carbon Dioxide Excretion
Ammonia Excretion
Blood Perfusate
Site Of Linkage
Ventilatory Water
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