Think you know all there is to know about marine teleost fish osmoregulation? Well, you might want to think again. You may be familiar with the fact that marine fish continuously drink seawater to counteract their constant water loss to the environment - a consequence of the dramatic difference in salt content between the extracellular fluid and the more concentrated seawater environment. You may also know that the marine teleost intestine plays an important role in osmoregulation, contributing to water balance through the absorption of fluids via the active transport of Na+ and Cl- in response to their high seawater consumption. But, did you know about the importance of intestinal Cl-/HCO3- exchange in osmoregulation? The secretion of HCO3- into the intestinal lumen contributes to the absorption of Cl- and water and is so substantial that it results in basic intestinal fluids with HCO3-concentrations high enough to precipitate solid calcium carbonate in the gut lumen. Incredibly, this `gut rock' phenomenon appears to be common to all fish living in a seawater environment, but until now the mechanism of Cl-/HCO3- exchange in fish intestine was relatively uncharacterized. In a recent study published in the American Journal of Physiology, Martin Grosell and Janet Genz have elucidated the details of intestinal Cl-/HCO3- exchange and determined its overall contribution to marine osmoregulation in the toadfish.

To measure HCO3- across the toadfish intestinal epithelium, Grosell and Genz took a segment of intestinal epithelia and divided an Ussing chamber in two with the lumen facing a chamber filled with a luminal fluid-like saline and the blood side of the tissue facing a chamber filled with a blood-like saline. As the intestinal epithelium secreted HCO3- into the luminal fluid, acid was titrated into the fluid to maintain the luminal pH at 7.8. The amount of acid added was equal to the amount of base secreted giving a direct measure of the tissue's HCO3- secretion. Using this approach, the temperature,pH and composition of the saline solutions in the chambers were manipulated and pharmacological agents, such as ATP or transport blockers, added to characterize the mechanism of HCO3- secretion.

The pair was able to determine that intestinal HCO3-secretion into the lumen occurs via a secondary active mechanism that is very sensitive to changes in temperature and requires energy in the form of ATP, which suggests that Cl-/HCO3- exchange in toadfish intestine is a transporter-mediated process. While half the total HCO3- secreted by the intestine appeared to come from either CO2 or HCO3- extracted from blood, the team determined that metabolic CO2 produced by the tissue accounted for the other half of HCO3- secretion. Furthermore,inhibiting the carbonic anhydrase inside the intestinal cell, which catalyzes CO2 and H2O to form HCO3- and H+, substantially reduced HCO3- secretion,suggesting that the hydration of CO2 is important to HCO3- secretion. Grosell and Genz determined that the acid (H+) from the hydration reaction was absorbed into the extracellular fluid on the blood-side of the intestine, likely through a Na+/H+ exchanger located on the basolateral (blood-side)membrane. They also found that the elimination of H+ from the intracellular space was necessary for the continued secretion of HCO3-. What is astounding about this finding is that the extrusion of H+ across the intestine's basolateral membrane results in the absorption of a very large acid load; the theoretical pH of the absorbed fluid was calculated as being close to 1!

As more details of Cl-/HCO3- exchange are revealed by the Grosell group, the similarities between Cl-/HCO3- exchangers in fish and mammals become more apparent. That being the case, it is likely that the teleost intestinal epithelium may provide a valuable model for mammalian HCO3- secretion and/or fluid absorbing epithelia. And you thought you knew everything...

Grosell, M. and Genz, J. Ouabain sensitive bicarbonate secretion and acid absorption by the marine teleost fish intestine play a role in osmoregulation.
Am. J. Physiol.