Nitrogenous waste excretion in resting dogfish occurred largely (>90 %) as urea-nitrogen (urea-N) efflux across the gills, with a very small urea efflux via the kidney. Ammonia excretion, almost entirely at the gills, accounted for less than 3 % of total nitrogen excretion. Given the extremely high blood urea levels (approximately 640 mmol-N l-1) 'retained' for osmoregulation, and blood ammonia levels (approximately 80 µmol-N l-1) comparable to those of teleosts, the gills of resting dogfish were exceptionally impermeable to both urea and ammonia. Experiments investigated the origins of these low permeabilities and the responses of urea-N and ammonia-N excretion and acid­base status to 6 h infusions with iso-osmotic solutions of NaCl (control), NH4Cl, NaHCO3, urea and its analogues thiourea and acetamide. NaCl had no effects, whereas NH4Cl loading caused intense acidosis and marked elevation of acidic equivalent, ammonia-N and urea-N excretion rates, the latter despite unchanged blood levels of urea-N. Apparent branchial ammonia permeability increased greatly. Acidosis resulted from both stimulated urea production and branchial NH3 loss, the former making the larger contribution. NaHCO3 loading caused intense alkalosis, a marked elevation of basic equivalent excretion and a moderate stimulation of urea-N excretion. Blood urea-N levels were again unchanged. Infusion of urea itself raised blood urea-N levels, but initially reduced branchial urea-N excretion. Acetamide and thiourea infusions both moderately elevated branchial urea-N excretion. We suggest that the low ammonia permeability may arise metabolically from an ammonia scavenging system in the gills, that a 'back-transport' mechanism in the gills may contribute to the low urea permeability, and that the dissociation between blood urea-N levels and excretion rates may reflect urea production at extrahepatic sites. These studies demonstrate that urea synthesis in the dogfish is linked more to nitrogen availability than to acid­base status.

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