MCCORMICK, Stephen D.*; O’DEA, Michael F.; MOECKEL, Amy M.; USGS, Conte Anadromous Fish Research Center, Turners Falls MA USA; Organismic and Evolutionary Biology Program, University of Massachusetts, Amherst USA: Are we missing a mineralocorticoid in fish? Effect of corticoids and receptor inhibitors on salinity tolerance of Atlantic salmon.

It has long been held that cortisol, acting through a single receptor, carries out both glucocorticoid and mineralocorticoid actions in teleost fish. The recent finding that fish possess a gene with high sequence similarity to the mammalian mineralocorticoid receptor, and has similar binding characteristics in the expressed protein, suggests the possibility that a hormone other than cortisol carries out some mineralocorticoid functions in fish. To test for this possibility, we examined the ability of cortisol, 11-deoxycorticosterone (DOC) and aldosterone to increase salinity tolerance in Atlantic salmon. In vivo cortisol treatment for 6 to 12 days that resulted in increased physiological levels of cortisol also resulted in increased gill Na,K-ATPase (NKA) activity and improved salinity tolerance (lower plasma chloride after a 24 h seawater challenge). Administration of DOC and aldosterone did not increase either NKA activity or salinity tolerance. RU486 effectively blocked the ability of cortisol to increase NKA activity and salinity tolerance, but spironolactone was only partially effective. Neither RU486 or spironolactone blocked changes in gill NKA activity or plasma chloride 6 days after transfer of fish from fresh water to seawater or from seawater to fresh water. The results provide support that cortisol, and not DOC or aldosterone, regulates salinity tolerance in salmonids, but do not rule out a role for DOC or aldosteroine in other osmoregulatory or physiological actions.