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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0281v1 203/2/301    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tipsmark, C. K Articles by Madsen, S. S PubMed PubMed Citation Articles by Tipsmark, C. K Articles by Madsen, S. S

Institute of Biology, University of Southern Denmark, Campusvej 55, DK-5230 Odense M, Denmark

(Correspondence should be addressed to C K Tipsmark; Email: ckt{at}biology.sdu.dk)

It has recently become evident that maintenance of ionic homoeostasis in euryhaline salmonids involves a reciprocal shift in expression of two isoforms of the gill Na⁺,K⁺-atpase -subunit when the surrounding salinity changes. The present study investigated the regulation of this shift between the 1a (freshwater (FW) isoform) and the 1b (seawater (SW) isoform) by cortisol, Gh, prolactin (Prl) and Igf 1. Injection with cortisol into FW salmon increased 1a expression, while Gh had no effect. Conversely, both cortisol and Gh stimulated 1b expression, and a significant synergy was observed. igf1 expression was increased by Gh in both gill and liver, and inhibited by cortisol in the liver. Gill igf1 and gh receptor expression increased in response to cortisol. Injection with Prl into SW salmon compromised their hypo-osmoregulatory performance, selectively reduced the expression of the 1b isoform and decreased enzymatic Na⁺,K⁺-atpase activity in the gill. Cortisol and Prl reduced gill and liver igf1 expression, and both hormones stimulated gill igf1 receptor expression. In a short-term experiment with incubation of FW gill cell suspensions, cortisol stimulated 1a and 1b expression, while Igf1 stimulated only 1b. The data elaborate our understanding of Prl and Gh as being antagonists in the control of gill ion regulation, and support a dual role for Gh involving endocrine and paracrine Igf1 action. Gh and Prl may be the decisive stimuli that direct cortisol-aided mitochondrion-rich cell development into either secretory or absorptive types.