We examined the relationship between plasma cortisol levels, hepatic glutamine synthetase (GNS) activity and the form of nitrogen excreted (e.g. urea, ammonia) in undisturbed versus confined/crowded (acutely stressed) gulf toadfish. Specifically, we tested the hypothesis that acute increases in plasma cortisol levels are required to trigger the increase in GNS activity induced by the confinement/crowding stress. Toadfish responded to the stress of confinement/crowding with an initial cortisol surge (approximately 37 ng ml-1 at 2 h), which was rapidly cleared and was indistinguishable from resting levels (approximately 10 ng ml-1 by 24 h). Treatment of fish with metyrapone (which inhibits cortisol synthesis) successfully blocked the acute 2 h confinement/crowding-induced surge in plasma cortisol levels. Additionally, GNS activity in confined fish 24 h after metyrapone injection also did not differ from that of control fish, indicating that acute GNS activation probably requires the earlier (2 h) cortisol peak. In post-absorptive fish, a strong relationship between total nitrogen excretion rate and plasma cortisol levels was evident. The percentage of nitrogen excreted as ammonia was inversely related to liver GNS activity. However, GNS activity explained only part (at most 57%) of the variability in the percentage of nitrogen excreted as ammonia/urea, suggesting that this is not the sole factor setting the degree of ureogenesis. When toadfish are fed, the relationships between total nitrogen excretion rate and cortisol levels, and between percentage nitrogen excreted as ammonia and GNS activity, are virtually absent. Taken together, our results indicate that a stress response may be only one of several mechanisms by which ureogenesis is activated in gulf toadfish.

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