Most fish get rid of nitrogen waste in the form of toxic ammonia, which is easily disposed of in water. And they get two bangs for each buck as they transport the toxin through Rhesus channels in the gill by importing sodium counter ions in exchange for the excreted ammonia waste. But what about marine elasmobranchs, such as sharks, rays and skates that convert ammonia waste into urea to protect themselves from dehydration in salty water? According to Michele Nawata, Pat Walsh and Chris Wood from the Bamfield Marine Sciences Centre, Canada, it was assumed that these fish wouldn't excrete ammonia across their gills, but it was not known whether they possess ammonia-transporting Rhesus channels in their tissues. Catching spiny dogfish sharks in the sea off British Columbia, the trio tested the animals' responses to environmental ammonia (p. 238).
Measuring ammonia excretion across the gill under normal conditions, the team was unsurprised to find that it was low, ensuring that the fish retained sufficient ammonia for urea production. However, when environmental levels of ammonia were high, the shark unexpectedly began taking ammonia on board and also increased urea production – although the animals were unable to store the excess urea so their urea excretion rates increased also. And when the team compared the dogfish's expression of Rhesus channel genes and enzymes involved in ammonia excretion with the expression patterns in freshwater bony fish, they found that the shark altered both expression patterns, but in different ways from the freshwater animals.
Having found that the dogfish's responses to high environmental ammonia differ radically from those of freshwater species, the team admits that they were surprised that dogfish appear to be able to extract ammonia from their surroundings. They say, ‘we propose that the gill of this nitrogen-limited predator is poised… to scavenge ammonia-N from the environment during high environmental ammonia to enhance urea-N synthesis’.