HCO₃^- secretion and CaCO₃ precipitation play major roles in intestinal water absorption in marine teleost fish in vivo

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 HCO ₃^- 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 CaCO ₃. 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 CaCO₃ precipitation. Further analysis suggested that Na ⁺-independent fluid absorption could be accounted for by net Cl ^- and H⁺ absorption (from Cl^-/HCO ₃^- exchange and CO₂ hydration, respectively). There was no evidence to suggest that CaCO₃ alone 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.