HCO3−secretion and CaCO3precipitation play major roles in intestinal water absorption in marine teleost fish in vivo

Abstract

The intestine of marine teleosts must effectively absorb fluid from ingested seawater to avoid dehydration. This fluid transport has been almost exclusively characterized as driven by NaCl absorption. However, an additional feature of the osmoregulatory role of the intestine is substantial net HCO3−secretion. This is suggested to drive additional fluid absorption directly (via Cl−/HCO3−exchange) and indirectly by precipitating ingested Ca2+as CaCO3, thus creating the osmotic gradient for additional fluid absorption. The present study tested this hypothesis by perfusing the intestine of the European flounder in vivo with varying [Ca2+]: 10 (control), 40, and 90 mM. Fractional fluid absorption increased from 47% (control) to 73% (90 mM Ca2+), where almost all secreted HCO3−was excreted as CaCO3. This additional fluid absorption could not be explained by NaCl cotransport. Instead, a significant positive relationship between Na+-independent fluid absorption and total HCO3−secretion was consistent with the predicted roles for anion exchange and CaCO3precipitation. Further analysis suggested that Na+-independent fluid absorption could be accounted for by net Cl−and H+absorption (from Cl−/HCO3−exchange and CO2hydration, respectively). There was no evidence to suggest that CaCO3alone was responsible for driving fluid absorption. However, by preventing the accumulation of luminal Ca2+it played a vital role by dynamically maintaining a favorable osmotic gradient all along the intestine, which permits substantially higher rates of solute-linked fluid absorption. To overcome the resulting hyperosmotic and highly acidic absorbate, it is proposed that plasma HCO3−buffers the absorbed H+(from HCO3−production), and consequently reduces the osmolarity of the absorbed fluid entering the body.