Meeting Abstract
Arginine vasotocin (AVT) has been implicated to regulate salinity tolerance in fish, but AVT’s mechanisms of action are not known. Here we examine AVT system interaction with salinity tolerance in the euryhaline Amargosa pupfish (Cyprinodon nevadensis). Pupfish acclimated to brackish water (7.5 ppt) were transferred to fresh water (0.3 ppt), seawater (35 ppt), or hypersaline (55 ppt) conditions. Fish transferred to both 35 ppt and 55 ppt exhibited elevated V1a-type receptor v1a2 mRNA levels in the gill within 24 h, although v1a2 transcripts returned to baseline levels within 4 days. This transient increase in v1a2 mRNAs suggests that AVT’s effects on the gill might be mediated by a V1a-type receptor. To test this idea further, pupfish acclimated to 7.5 ppt were injected intraperitoneally with either a saline control, 1 μg AVT per g body mass, or 3.5 μg per g mass of a V1-type receptor antagonist (Manning compound). Immediately following injection, fish were either returned to 7.5 ppt or transferred to 0.3 or 35 ppt. Gene transcripts encoding the cystic fibrosis transmembrane conductance regulator (CFTR) in the gill epithelium increased in relative abundance 24 h after transfer to 35 ppt, but the magnitude of this increase was diminished in fish treated with Manning compound. No effect of Manning compound or AVT was observed on Na+/K+-ATPaseα1 subunit or Na+/K+/2Cl–cotransporter-1 mRNAs, which were also elevated in 35 ppt, or on aquaporin-3 mRNA, which became elevated in fish transferred to 0.3 ppt. The results indicate that AVT acting through the V1a-type receptor is involved in upregulation of CFTR during acclimation to elevated environmental salinity.
