Te. Hopkins et al., INTERACTIONS OF CORTISOL AND NITROGEN-METABOLISM IN THE UREOGENIC GULF TOADFISH OPSANUS-BETA, Journal of Experimental Biology, 198(10), 1995, pp. 2229-2235
We examined the relationship between plasma cortisol levels, hepatic g
lutamine synthetase (GNS) activity and the form of nitrogen excreted (
e.g. urea, ammonia) in undisturbed versus confined/crowded (acutely st
ressed) gulf toadfish. Specifically, we tested the hypothesis that acu
te increases in plasma cortisol levels are required to trigger the inc
rease in GNS activity induced by the confinement/crowding stress. Toad
fish responded to the stress of confinement/crowding with an initial c
ortisol surge (approximately 37 ng ml(-1) at 2 h), which was rapidly c
leared 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/cr
owding-induced surge in plasma cortisol levels. Additionally, GNS acti
vity in confined fish 24 h after metyrapone injection also did not dif
fer from that of control fish, indicating that acute GNS activation pr
obably requires the earlier (2 h) cortisol peak. In post-absorptive fi
sh, a strong relationship between total nitrogen excretion rate and pl
asma cortisol levels was evident. The percentage of nitrogen excreted
as ammonia was inversely related to liver GNS activity. However, GNS a
ctivity explained only part (at most 57%) of the variability in the pe
rcentage 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 c
ortisol levels, and between percentage nitrogen excreted as ammonia an
d GNS activity, are virtually absent. Taken together, our results indi
cate that a stress response may be only one of several mechanisms by w
hich ureogenesis is activated in gulf toadfish.