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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 esophagealnhe2or−3expression during smoltification; however,nhe3increased following 48 h of SW exposure in May. Esophagealnhe2, −3, andgrowth hormone receptor b1were elevated in smolts acclimated to SW for 2.5 weeks. Treatment with cortisol stimulated branchial Na⁺/K⁺‐ATPase (Nka) activity, andNa⁺/K⁺/2Cl⁻cotransporter 1(nkcc1),cystic fibrosis transmembrane regulator 1 (cftr1), andnka‐α1bexpression. Esophagealnhe2, but notnhe3expression, was stimulated by cortisol. In anterior intestine, cortisol stimulatednkcc2, cftr2, andnka‐α1b. Our findings indicate that salinity stimulates esophagealnhe2and−3, and that cortisol coordinates the expression of esophageal, intestinal, and branchial solute transporters to support the SW adaptability of Atlantic salmon.

 

Prolactin (PRL) cells within the rostral pars distalis (RPD) of euryhaline and eurythermal Mozambique tilapia, Oreochromis mossambicus, rapidly respond to a hyposmotic stimulus by releasing two distinct PRL isoforms, PRL 188 and PRL 177 . Here, we describe how environmentally relevant temperature changes affected mRNA levels of prl 188 and prl 177 and the release of immunoreactive prolactins from RPDs and dispersed PRL cells. When applied under isosmotic conditions (330 mosmol/kgH 2 O), a 6°C rise in temperature stimulated the release of PRL 188 and PRL 177 from both RPDs and dispersed PRL cells under perifusion. When exposed to this same change in temperature, ∼50% of dispersed PRL cells gradually increased in volume by ∼8%, a response partially inhibited by the water channel blocker, mercuric chloride. Following their response to increased temperature, PRL cells remained responsive to a hyposmotic stimulus (280 mosmol/kgH 2 O). The mRNA expression of transient potential vanilloid 4, a Ca 2+ -channel involved in hyposmotically induced PRL release, was elevated in response to a rise in temperature in dispersed PRL cells and RPDs at 6 and 24 h, respectively; prl 188 and prl 177 mRNAs were unaffected. Our findings indicate that thermosensitive PRL release is mediated, at least partially, through a cell-volume-dependent pathway similar to how osmoreceptive PRL release is achieved.