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We characterized the physiological effects of exposure to pH9.5 on one domesticated and four wild strains of diploid and triploid juvenile rainbow trout (Oncorhynchus mykiss) over two consecutive years. In the first year, 35-70% of the individuals from the wild strains showed a loss of equilibrium (LOE) at 12 h exposure to pH9.5, with all fish from wild strains experiencing a LOE by 48 h. In contrast, <20% of the domesticated strain showed LOE over the 48 h exposure to pH9.5. In our second experiment, similar strain effects were observed, but far fewer fish showed LOE (≤50% in all strains) over 72 h at pH9.5. In both experiments, there was no effect of ploidy on time to LOE. In the fish that did not show LOE, high pH exposure resulted in significant increases in plasma, brain and muscle ammonia, with no effect of strain or ploidy on the extent of ammonia accumulation. Glutamine accumulated in the brain during high pH exposure, with a stoichiometric decrease in glutamate, but no differences were noted among strains or ploidies. Lactate also accumulated in the plasma to a similar extent in all trout strains and ploidies. Plasma chloride decreased at 24h exposure in all trout strains and ploidies, but recovered by 72 h. No change was observed in plasma sodium. Overall, our data suggest that the domesticated strain of trout is more tolerant of pH9.5 than the wild strains, but these differences in tolerance cannot be explained by our sub-lethal assessment of ammonia balance or ion regulation., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Ureotelic Gulf toadfish (Opsanus beta) do not excrete urea continuously; instead, urea is accumulated internally until a branchial urea transport mechanism is activated to facilitate the excretion of urea in distinct pulses. This unusual pulsatile urea excretion pattern is regulated, in part, by permissive declines in circulating cortisol concentrations. The current study examined toadfish urea transporter (tUT) and glucocorticoid receptor (GR) transcript levels in toadfish gill following chronic (days) and acute (hours) changes in corticosteroid activity. Experimentally lowering circulating cortisol did not significantly alter tUT mRNA abundance but increased GR mRNA. On an acute timescale, a 6.2-fold upregulation of tUT mRNA occurred 12 to 18 h following a urea pulse event with no change in GR mRNA. In silico analysis of an isolated 1.2 kb fragment, upstream promoter region of the tUT gene, revealed 6 putative glucocorticoid response element (GRE) half sites. In vivo reporter assays of the tUT promoter fragment demonstrated relative luciferase activity was enhanced 3.4- and 9.8-fold following exposure to moderate (via a 48 h crowding stress) and high (via infusion for 48 h) cortisol. We conclude that a GRE-mediated upregulation of mRNA may be required to maintain tUT activity by offsetting post-transcriptional and/or post-translational changes that may be associated with chronically elevated plasma cortisol., (Copyright © 2011 Elsevier Inc. All rights reserved.)