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Pulsatile urea excretion in the toadfish (Opsanus beta) is due to a pulsatile excretion mechanism, not a pulsatile
Abstract:
When subjected to a crowding/confinement protocol in the laboratory, toadfish become facultatively ureotelic, excreting approximately 90 % of their nitrogenous waste as urea-nitrogen (urea-N). The great majority of this excretion occurs via large, irregular pulses from the head region which occur on average once per day, with a duration of 3 h or less. Pulses measured chemically by the appearance of urea-N in the external water were identical to those measured by assaying [14C]urea appearance in the water from the blood plasma. Individual toadfish maintained plasma urea concentrations over widely differing ranges (660039 890 µmol-N l-1). However, independent of absolute levels, both [14C]urea and total urea were distributed at ratios close to unity between the blood plasma and the water compartments of liver and white muscle. At times of pulsatile excretion, plasma urea concentration fell sharply. These decreases, distributed throughout the tissues of the whole body, closely matched the sizes of the measured excretion pulses. Between pulses, plasma urea concentration increased steadily at a much slower rate; the rate of rise, when distributed throughout the tissues of the whole body, corresponded to the time-averaged excretion rate over the whole day. Infusion of a typical pulse amount of urea immediately after the end of a natural pulse event raised plasma urea concentration slightly above the pre-pulse level, but did not induce another pulse event. Plasma cortisol levels declined by approximately 60 % over the 4 h period prior to a natural pulse event and then rose quickly again once the pulse had occurred. These results indicate that urea pulses are due to activation of an excretion mechanism that rapidly clears urea from the blood plasma, thereby lowering stores throughout the whole body. Metabolic production of urea is continuous and is not responsible for pulsatile excretion. The pulse event is not triggered by a specific plasma urea threshold, but may involve the hypothalamointerrenal axis.