Intestinal HCO3- secretion is essential to marine teleost fish osmoregulation and comprises a considerable source of base efflux attributable to both serosal HCO3- and endogenous CO2 hydration. The role of intestinal HCO3- secretion in dynamic acid-base balance regulation appears negligible in studies of unfed fish, but evidence of high intestinal fluid [HCO3-] in fed marine teleosts led us to investigate the source of this HCO3- and its potential role in offsetting the postprandial 'alkaline tide' commonly associated with digestion. Specifically, we hypothesized that elevated metabolic rate and thus endogenous CO2 production by intestinal tissue as well as increased transepithelial intestinal HCO3- secretion occur post-feeding and offset a postprandial alkaline tide. To test these hypotheses changes in HCO3- secretion and O2 consumption by gulf toadfish (Opsanus beta) isolated intestine were quantified 0, 3, 6, 12, 24 and 48 h post-feeding. Intestinal tissue of unfed fish in general showed high rates of HCO3- secretion (15.5 mumol g(-1) h(-1)) and O2 consumption (8.9 mumol g(-1) h(-1)). Furthermore, postprandial increases in both intestinal HCO3- secretion and O2 consumption (1.6- and 1.9-fold peak increases, respectively) were observed. Elevated intestinal HCO3- secretion rates preceded and outlasted those of O2 consumption, and occurred at a magnitude and duration sufficient to account for the lack of alkaline tide. The dependence of these high rates of postprandial intestinal base secretion on serosal HCO3- indicates transepithelial HCO3- transport increases disproportionately more than endogenous CO2 production. The magnitude of postprandial intestinal HCO(3)(-) secretion indicates the intestine certainly is capable of postprandial acid-base balance regulation.