Salt Water and Acid - Base Balance

Gulf toadfish in the lab resting in PVC tube Gulf toadfish in the lab resting in PVC tube
Gulf toadfish perching on another in the lab Gulf toadfish perching on another in the lab
Two Gulf Toadfish resting in a PVC tube Two Gulf Toadfish resting in a PVC tube
Gulf toadfish swimming in lab tank Gulf toadfish swimming in lab tank
Marine fish live in a desiccating environment and must constantly combat fluid loss by drinking seawater. The ingested seawater is desalinized in the esophagus, allowing for fluid absorption by the intestine. In the intestine, water uptake is coupled to sodium and chloride absorption. One specific aspect of this process that is of great interest to our lab is that during water absorption, chloride is taken up into the intestine in exchange for bicarbonate. Consequently, the intestinal fluid of marine fish contains elevated luminal concentrations of HCO3-. This presence of elevated Ca2+ ingested with seawater combined with the elevated luminal HCO3- concentrations and alkaline pH creates favorable conditions for the precipitation of CaCO3 in the intestinal lumen. Importantly, the conversion of ions to CaCO3 reduces the osmotic pressure of intestinal fluids by as much as 100 mOsm, making this process crucial to osmoregulation in seawater. In fact, all marine fish examined to date perform this process, underscoring its central role in permitting fish thrive in salty environments. The ultimate fate of the precipitated CaCO3 is release to the environment whereby marine fish contributes by up to 15% of the global oceanic CaCO3 production and the inorganic carbon cycle (Wilson et al 2009) (Fig 1). Intestinal base secretion in form of HCO3- and CaCO3 release is not involved in dynamic acid-base balance regulation but contributes to the overall acid-base balance and is elevated during exposures to elevated salinity (Genz et al 2011), temperature (Heuer et al 2016) and partial pressure of CO2 (see below) as well as during digestion (Taylor & Grosell 2009). Such elevations in intestinal base secretion alter blood acid-base status and are compensated by the gills (Genz et al 2008).