Abstract

Stress and elevated cortisol levels are associated with pathological heart growth and cardiovascular disease in humans and other mammals. We recently established a link between heritable variation in post-stress cortisol production and cardiac growth in salmonid fish too. A conserved stimulatory effect of the otherwise catabolic steroid hormone cortisol is probably implied, but has to date not been established experimentally. Furthermore, whereas cardiac growth is associated with failure of the mammalian heart, pathological cardiac hypertrophy has not previously been described in fish. Here, we show that rainbow trout (Oncorhynchus mykiss) treated with cortisol in the diet for 45 days have enlarged hearts with lower maximum stroke volume and cardiac output. In accordance with impaired cardiac performance, overall circulatory oxygen-transporting capacity was diminished as indicated by reduced aerobic swimming performance. In contrast to the well-known adaptive/physiological heart growth observed in fish, cortisol-induced growth is maladaptive. Furthermore, the observed heart growth was associated with up-regulated signature genes of mammalian cardiac pathology, suggesting that signalling pathways mediating cortisol-induced cardiac remodelling in fish are conserved from fish to mammals. Altogether, we show that excessive cortisol can induce pathological cardiac remodelling. This is the first study to report and integrate the etiology, physiology and molecular biology of cortisol-induced pathological remodelling in fish.

Keywords

Myocardial hypertrophy; Chronic stress; Heart failure; Rainbow trout; Cardiac performance

Published in

Journal of Experimental Biology
2017, Volume: 220, number: 14, pages: 2545-2553

SLU Authors

• Gräns, Albin

  • Department of Applied Animal Science and Welfare, Swedish University of Agricultural Sciences
    

UKÄ Subject classification

Other Veterinary Science


Publication identifier

DOI: https://doi.org/10.1242/jeb.135046

Permanent link to this page (URI)

https://res.slu.se/id/publ/86743