Meeting Abstract
The homologous peptides guanylin, uroguanylin, and renoguanylin (RGN) affect osmoregulation in the posterior intestine of the Gulf toadfish by reversing short-circuit current, due to net Cl– secretion, which leads to fluid secretion and inhibition of HCO3– secretion, and is likely facilitated by basolateral NKCC1 and apical CFTR in the posterior intestine. These observations contradict the established osmoregulatory function of the marine teleost intestine in fluid absorption, but may facilitate the release of CaCO3 precipitates. To test this hypothesis, fish were exposed to hypersalinity (60 ppt), which increases intestinal CaCO3 production. At 60 ppt, the posterior intestine expressed elevated mRNA for NKCC1, CFTR, and the guanylin peptides’ receptor, and resulted in a greater secretory response to RGN by this tissue, in support of the above hypothesis. To test whether the elevated HCO3– secretion in 60 ppt is due to increased transport by the basolateral Na+/ HCO3–-cotransporter (NBCe1) or increased CO2 production by the enterocytes, HCO3–-free serosal saline was exchanged for serosal saline during experiments. Results demonstrate an expected decrease in HCO3– secretion in tissues after serosal saline was exchanged with HCO3–-free serosal saline, confirming transepithelial HCO3– secretion via NBCe1. Conversely, tissues exposed to 60 ppt revealed higher HCO3– secretion rates than control tissues in absence of serosal HCO3–, indicating a higher metabolic rate. Moreover, when in the absence of serosal HCO3–, RGN decreased baseline HCO3– secretion in tissues exposed to either treatment, suggesting action on apical HCO3– transporters.
