| Summary: | Intestinal HCO3- secretion and the excretion of resultant CaCO3 precipitates have become a recognized characteristic of seawater osmoregulation in teleosts; however, this is the first report of this osmoregulatory strategy outside of teleosts and also includes evidence for its use in green turtles, Chelonia mydas. Furthermore, the effects of feeding on intestinal HCO3- secretion were newly investigated in teleosts. Intestinal base secretion via apical Cl-/HCO3- exchange was found to increase following feeding, at a magnitude sufficient to offset the "alkaline tide" commonly associated with digestion. Intestinal HCO3- secretion in marine teleosts draws HCO3- from both endogenous (via hydration of intracellular CO2) and serosal (blood) sources, of which serosal HCO3- was found to contribute a greater proportion to the elevated postprandial intestinal base secretion measured in gulf toadfish, Opsanus beta. The mechanism by which this serosal HCO3- crosses the basolateral membrane for subsequent secretion into the intestinal lumen was confirmed in toadfish to be a basolateral Na+/HCO3- co-transporter, tfNBCe1. Furthermore, the isolated intestinal tissue was found to have a high metabolic rate in both control and postprandial toadfish, with respect to that of the whole animal, and shows a considerable specific dynamic action (SDA) response to feeding. Overall, this dissertation provides evidence for the widespread use of intestinal HCO3- secretion as a strategy of marine osmoregulation across aquatic taxa, and also for its newly recognized involvement in postprandial acid-base balance.
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