Effects of growth hormone and insulin-like growth factor I on salinity tolerance and gill Na+, K+-ATPase in Atlantic salmon (Salmo salar): interaction with cortisol.

The potential roles of growth hormone (GH) and insulin-like growth factor I (IGF-I) in seawater (SW) acclimation of juvenile Atlantic salmon (Salmo salar) were examined. Compared to controls, fish in 12 ppt seawater given one or three injections (2-6 days) of GH (ovine, 0.2 microgram.g-1) or IGF-I (recombinant bovine, 0.05-0.2 microgram.g-1) had significantly greater salinity tolerance as judged by lower plasma sodium, osmolality, and muscle moisture content following transfer to 34 ppt. Single injections of GH and IGF-I in fish in fresh water failed to improve salinity tolerance following transfer to 25 ppt SW. Treatment of fish in 12 ppt with GH or IGF-I for 2-6 days did not increase gill Na+, K(+)-ATPase activity, but treatment with GH prevented decreases in gill Na+, K(+)-ATPase activity that occurred in controls following transfer to 34 ppt seawater. Fish in fresh water administered GH by implants (5.0 microgram.g-1) or osmotic minipumps (0.5 micrograms.g-1 day-1) for 7-14 days had greater gill Na+, K(+)-ATPase activity and salinity tolerance than controls. IGF-I administered by implants (0.5-1.0 microgram.g-1) or osmotic minipumps (0.1 microgram.g-1 day-1) for 4-14 days did not increase salinity tolerance or gill Na+, K(+)-ATPase activity. Cortisol implants (50 micrograms.g-1) also increased gill Na+, K(+)-ATPase activity and salinity tolerance after 14 days, and in combination with GH had a synergistic effect, Although IGF-I and cortisol implants had no significant effect after 7 days, in combination they significantly increased gill Na+, K(+)-ATPase activity. The results indicate that GH and cortisol can increase salinity tolerance and gill Na+, K(+)-ATPase activity of Atlantic salmon and together act in synergy. Although IGF-I can increase salinity tolerance in short-term treatments (2-6 days) in 12 ppt, it is less effective than GH in increasing salinity tolerance and gill Na+, K(+)-ATPase activity in long-term treatments (7-14 days) and in interacting with cortisol.