MCDONALD, M. Danielle; WALSH, Patrick J.; Rosenstiel School and Marine and Atmospheric Science, University of Miami; Rosenstiel School of Marine and Atmospheric Science, University of Miami: The role of glucocorticoids and 5-HT₂-like receptors in branchial urea excretion of the gulf toadfish, Opsanus beta

The gulf toadfish, Opsanus beta, has a unique pulsatile urea excretion mechanism that allows it to excrete its daily urea production in distinct 1-3 hour urea pulses rather than allowing the urea to leak continuously across the gill. In mammals and other organisms, urea passes across epithelia with the help of facilitated diffusion urea transporters (UT). In toadfish, tUT is activated or inserted into the gill membrane periodically, which causes a pulsatile and not continuous increase in urea permeability. Circulating glucocorticoids appear to play an inhibitory role in the regulation of tUT; immediately before a urea pulse circulating cortisol concentrations drop, allowing the activation of tUT, and then cortisol levels rise immediately after the pulse. In addition, intravenous cortisol infusion causes a reduction in urea excretion. In contrast, serotonin (5-HT; 5-hydroxytryptamine), mediated by 5-HT₂-like receptors, appears to be responsible for the activation of tUT as intravenous injections of 5-HT and the 5-HT₂ receptor agonist, α-methyl 5-HT, triggers a urea pulse. Ketanserin, a 5-HT_2A receptor antagonist, blocks the action of α-methyl 5-HT. The interaction between glucocorticoids and 5-HT and the effect they have on the regulation of tUT will be outlined.