Effects of elevated circulating cortisol levels on hydromineral status and gill tight junction protein abundance in the stenohaline goldfish

A role for cortisol in the regulation of hydromineral balance and gill tight junction (TJ) protein transcript abundance in the stenohaline freshwater goldfish was investigated. Intraperitoneal cortisol implants (50, 100, 200, 400 μg cortisol/g body weight) were used to dose-dependently elevate circulating cortisol levels over a 4 day period. Elevated cortisol did not significantly alter serum osmolality, serum Na+ or muscle water content, however serum glucose and gill Na+–K+-ATPase activity were significantly increased and serum Cl− levels were significantly reduced when compared to control groups. Transcript levels for glucocorticoid receptor 1 (GR1) and mineralocorticoid receptor (MR) in the gill remained unchanged by cortisol treatment, however glucocorticoid receptor 2 (GR2) mRNA abundance was significantly down-regulated. Conversely, cortisol treatment significantly increased transcript and protein abundance of the TJ protein occludin in goldfish gill tissue, as well as mRNA abundance for claudin e, 7 and 8d. Goldfish tissue expression profiles demonstrated that transcripts encoding for these claudins are particularly abundant in the gill. Overall, results suggest a ‘tightened’ gill epithelium in response to elevated cortisol levels in goldfish. However, negative autoregulation of gill GR2 transcript suggests a lessened capacity to respond to cortisol and thus a potentially ‘dampened’ corticosteroid-mediated effect in the gill. Reduced systemic Cl− levels also suggest that sustained cortisol elevation in goldfish may have a detrimental effect on other ionoregulatory tissues.

► Effects of elevated circulating cortisol levels were studied in goldfish.
► Serum osmolality, Na+ and muscle water content were unaffected by elevated cortisol.
► Elevated cortisol reduced serum Cl− and increased serum glucose levels.
► Gill Na+–K+-ATPase activity, occludin and claudin e, 7 and 8d abundance increased.
► Results suggest cortisol-mediated salt loss across non-gill ionoregulatory tissues.