In marine habitats, Atlantic salmon (Salmo salar) imbibe seawater (SW) to replace body water that is passively lost to the ambient environment. By desalinating consumed SW, the esophagus enables solute-linked water absorption across the intestinal epithelium. The processes underlying esophageal desalination in salmon and their hormonal regulation during smoltification and following SW exposure are unresolved. To address this, we considered whether two Na+ /H+ exchangers (Nhe2 and -3) expressed in the esophagus contribute to the uptake of Na+ from lumenal SW. There were no seasonal changes in esophageal nhe2 or -3 expression during smoltification; however, nhe3 increased following 48 h of SW exposure in May. Esophageal nhe2, -3, and growth hormone receptor b1 were elevated in smolts acclimated to SW for 2.5 weeks. Treatment with cortisol stimulated branchial Na+ /K+ -ATPase (Nka) activity, and Na+ /K+ /2Cl- cotransporter 1 (nkcc1), cystic fibrosis transmembrane regulator 1 (cftr1), and nka-α1b expression. Esophageal nhe2, but not nhe3 expression, was stimulated by cortisol. In anterior intestine, cortisol stimulated nkcc2, cftr2, and nka-α1b. Our findings indicate that salinity stimulates esophageal nhe2 and -3, and that cortisol coordinates the expression of esophageal, intestinal, and branchial solute transporters to support the SW adaptability of Atlantic salmon.
Keywords: cortisol; esophagus; gill; growth hormone; intestine; receptor; smoltification.
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