title: Cortisol response to stress is associated with myocardial remodeling in salmonid fishes.
abstract: Cardiac disease is frequently reported in farmed animals, and stress has been implicated as a factor for myocardial dysfunction in commercial fish rearing. Cortisol is a major stress hormone in teleosts, and this hormone has adverse effects on the myocardium. Strains of rainbow trout (Oncorhynchus mykiss) selected for divergent post-stress cortisol levels [high responsive (HR) and low responsive (LR)] have been established as a comparative model to examine how fish with contrasting stress-coping styles differ in their physiological and behavioral profiles. We show that the mean cardiosomatic index (CSI) of adult HR fish was 34% higher than in LR fish, mainly because of hypertrophy of the compact myocardium. To characterize the hypertrophy as physiological or pathological, we investigated specific cardiac markers at the transcriptional level. HR hearts had higher mRNA levels of cortisol receptors (MR, GR1 and GR2), increased RCAN1 levels [suggesting enhanced pro-hypertrophic nuclear factor of activated T-cell (NFAT) signaling] and increased VEGF gene expression (reflecting increased angiogenesis). Elevated collagen (Col1a2) expression and deposition in HR hearts supported enhanced fibrosis, whereas the heart failure markers ANP and BNP were not upregulated in HR hearts. To confirm our results outside the selection model, we investigated the effect of acute confinement stress in wild-type European brown trout, Salmo trutta. A positive correlation between post-stress cortisol levels and CSI was observed, supporting an association between enhanced cortisol response and myocardial remodeling. In conclusion, post-stress cortisol production correlates with myocardial remodeling, and coincides with several indicators of heart pathology, well-known from mammalian cardiology.
authors: Department of Animal and Aquacultural Sciences, Norwegian University of Life Sciences (UMB), 0476 Ås, Norway. ida.johansen@umb.no
authors: Ida B
authors: IB
authors: Johansen
authors: Ida G
authors: IG
authors: Lunde
authors: Helge
authors: H
authors: Røsjø
authors: Geir
authors: G
authors: Christensen
authors: Göran E
authors: GE
authors: Nilsson
authors: Morten
authors: M
authors: Bakken
authors: Oyvind
authors: O
authors: Overli
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D006984:Hypertrophy; D009206:Myocardium / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D050778:NFATC Transcription Factors / Q000235:genetics / Q000378:metabolism; D020097:Natriuretic Peptide, Brain / Q000235:genetics / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000235:genetics / Q000378:metabolism; D012487:Salmonidae / Q000033:anatomy & histology / Q000502:physiology*; D013312:Stress, Physiological; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D015415:Biomarkers; D050778:NFATC Transcription Factors; D011965:Receptors, Glucocorticoid; C029360:hydrocortisone receptor; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor; D003094:Collagen; D006854:Hydrocortisone