The possible presence of a urea transporter in the kidney of the gulf toadfish (Opsanus beta) and further characterization of the pulsatile facilitated transporter previously identified in its gills were investigated by comparing the extra-renal and renal handling of two urea analogues with the handling of urea. Toadfish were fitted with caudal artery and indwelling urinary ureteral catheters and injected with an iso-osmotic dose of (14)C-labelled urea analogue (acetamide or thiourea) calculated to bring plasma analogue concentrations close to plasma urea concentrations. Branchial permeabilities to urea, acetamide and thiourea were similar during non-pulsing periods and all increased during pulse events, although urea permeability was greater than analogue permeability during pulses. The incidence and magnitude of acetamide and urea pulses at the gills were significantly correlated, acetamide pulses being 35-50 % of the size of urea pulses. However, the thiourea and urea pulses at the gills were only weakly correlated, thiourea pulses being less than 16 % of the size of urea pulses. Thiourea inhibited branchial urea excretion by reducing the pulse frequency. The renal handling of thiourea and urea were similar in that both substances were more concentrated in the urine than in the plasma, whereas acetamide was found in equal concentrations in the urine and plasma. Urea and thiourea were secreted 2-3 times more effectively than Cl(-) and water, whereas acetamide was secreted at a similar relative rate. The differential handling of the urea analogues by the gills and kidney indicates the presence of a different, possibly unique, transporter in the kidney. The movement of thiourea and urea into the renal tubule against an apparent concentration gradient suggests the presence of an active transport mechanism.