Intestinal bicarbonate secretion in marine teleost fish—source of bicarbonate, pH sensitivity, and consequences for whole animal acid–base and calcium homeostasis

AbstractWhole animal studies using seawater European flounder (Platichthys flesus) revealed that increasing intestinal [Ca2+] to 20 mM stimulated net HCO3− base secretion by 57%, but this was effectively balanced by an increase in net acid secretion, likely from the gills, to maintain whole animal acid–base status. Higher Ca2+ concentrations (40 and 70 mM) in ambient seawater resulted in reduced plasma total CO2. This indicates (1) imperfect acid–base compensation, and (2) that endogenous metabolic CO2 is insufficient to fuel intestinal HCO3− secretion, under hyper-stimulated conditions. Bicarbonate secretion plays an important role in preventing calcium absorption by precipitating a large fraction of the imbibed calcium as CaCO3. Indeed, under high Ca2+ conditions (20 mM), up to 75% of the intestinal Ca2+ is precipitated as CaCO3 and then excreted. This is undoubtedly important in protecting the marine teleost kidney from the need for excessive calcium excretion and risk of renal stone formation. Using an in vitro pH-stat technique with the isolated intestinal epithelium, the replacement of serosal CO2 with a HEPES buffered saline had no effect on HCO3− secretion, indicating that the endogenous supply of HCO3− from CO2 hydration within epithelial cells is adequate for driving baseline secretion rates. Further, in vitro data demonstrated a stimulatory effect of low pH on intestinal HCO3− secretion. Thus, both luminal Ca2+ and H+ can regulate HCO3− secretion but the precise mechanisms and their potential interaction are currently unresolved