Do circulating plasma AVT and/or cortisol levels control pulsatile urea excretion in the gulf toadfish (Opsanus beta)?

Previous work has shown that pulsatile urea excretion at the gills of the g ulf toadfish is due to periodic activation of a facilitated diffusion trans port system with molecular and pharmacological similarity to the UT-A trans port system of the mammalian kidney. In mammals, AVP and glucocorticoids ar e two important endocrine regulators of this system. The present study focu sed on the potential role of circulating AVT (the teleost homologue of AVP) and cortisol levels as possible triggers for urea pulses. Long-term (34-84 h) monitoring of plasma levels by repetitive sampling at 2-h intervals fro m chronic cannulae in individual toadfish demonstrated that circulating AVT concentrations are low (10(-12)-10(-11) M), and show no relationship to th e occurrence of natural urea pulses. In contrast, plasma cortisol levels de cline greatly prior to natural pulses and rise rapidly thereafter. AVT inje ctions into the caudal artery or ventral aorta elicited pulse events, but t hese were extremely small(1-10%) relative to natural pulses, and occurred o nly at unphysiological dose levels (10(-9) M in the plasma). AVP was a part ial agonist, but isotocin, insulin-like growth factor-1, and atrial natriur etic peptide were without effect at the same concentration. Artificially ra ising plasma cortisol levels by cortisol injection tended to reduce respons iveness to AVT, Pharmacological reduction of plasma cortisol levels by mety rapone injection elicited small pulses similar to those caused by AVT. Foll owing such pulse events, AVT was ineffective in inducing pulses. We conclud e that decreases in circulating cortisol play an important permissive role in urea pulsing, but that circulating AVT levels are not involved. (C) 2001 Elsevier Science Inc. All rights reserved.