Mineralocorticoid receptors and ionic regulation in rainbow trout (Oncorhynchus mykiss)

Abstract

The mineralocorticoid receptor (MR) was recently cloned from two fish species, Haplochromis burtoni (H. burtoni; hbMR) and rainbow trout (Oncorhynchus mykiss; rtMR). The objectives of the present study were to detect MR protein expression in rainbow trout ionoregulatory tissues, namely the gill and kidney, as well as to use the mammalian MR agonist aldosterone to selectively target and activate the rainbow trout MR to observe its effects on renal and branchial ionic regulation. Through immunohistochemistry and Western blot analysis using a heterologous antibody, MR protein expression was detected at the gill. Immunohistochemical analysis and flow cytometry data indicated that there was a high degree of colocalization of the rtMR to Na+-K+-ATPase rich cells at the gill, supporting the hypothesis that the rtMR is involved in branchial ionic regulation. Additionally, acute aldosterone treatment, but not cortisol treatment, stimulated a decrease in urine flow rate (UFR) and urinary sodium excretion at 1.5 h post-injection. The decrease in UFR occurred without any change in glomerular filtration rate (GFR), suggesting that the aldosterone-induced decrease in UFR was the result of increased tubular reabsorption of water, which in turn was presumably stimulated by enhanced Na+ reabsorption. The results of this study support the hypothesis that the rtMR is involved in renal and branchial ionic regulation and help to clarify the mechanisms through which corticosteroid-mediated ionic regulation occurs in euryhaline teleosts.