Pulsatile urea excretion in the gulf toadfish

Mechanisms and controls

Chris M. Wood, Danielle M Mcdonald, Lena Sundin, Pierre Laurent, Patrick J. Walsh

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Opsanus beta expresses a full complement of ornithine-urea cycle (OUC) enzymes and is facultatively ureotelic, reducing ammonia-N excretion and maintaining urea-N excretion under conditions of crowding/confinement. The switch to ureotelism is keyed by a modest rise in cortisol associated with a substantial increase in cytosolic glutamine synthetase for trapping of ammonia-N and an upregulation of the capacity of the mitochondrial OUC to use glutamine-N. The entire day's urea-N production is excreted in 1 or 2 short-lasting pulses, which occur exclusively through the gills. The pulse event is not triggered by an internal urea-N threshold, is not due to pulsatile urea-N production, but reflects pulsatile activation of a specific branchial excretion mechanism that rapidly clears urea-N from the body fluids. A bidirectional facilitated diffusion transporter, with pharmacological similarity to the UT-A type transporters of the mammalian kidney, is activated in the gills, associated with an increased trafficking of dense-cored vesicles in the pavement cells. An 1814 kB cDNA ('tUT') coding for a 475-amino acid protein with approximately 62% homology to mammalian UT-A's has been cloned and facilitates phloretin-sensitive urea transport when expressed in Xenopus oocytes. tUT occurs only in gill tissue, but tUT mRNA levels do not change over the pulse cycle, suggesting that tUT regulation occurs at a level beyond mRNA. Circulating cortisol levels consistently decline prior to a pulse event and rise thereafter. When cortisol is experimentally clamped at high levels, natural pulse events are suppressed in size but not in frequency, an effect mediated through glucocorticoid receptors. The cortisol decline appears to be permissive, rather than the actual trigger of the pulse event. Fluctuations in circulating AVT levels do not correlate with pulses; and injections of AVT (at supraphysiological levels) elicit only minute urea-N pulses. However, circulating 5-hydroxytryptamine (5-HT) levels fluctuate considerably and physiological doses of 5-HT cause large urea-N pulse events. When the efferent cranial nerves to the gills are sectioned, natural urea pulse events persist, suggesting that direct motor output from the CNS to the gill is not the proximate control.

Original languageEnglish
Pages (from-to)667-684
Number of pages18
JournalComparative Biochemistry and Physiology - B Biochemistry and Molecular Biology
Volume136
Issue number4
DOIs
StatePublished - Dec 1 2003

Fingerprint

Batrachoidiformes
Urea
Hydrocortisone
Ornithine
Ammonia
Serotonin
Facilitated Diffusion
Phloretin
Glutamate-Ammonia Ligase
Messenger RNA
Crowding
Cranial Nerves
Body fluids
Glucocorticoid Receptors
Body Fluids
Xenopus
Glutamine
Pavements
Oocytes

Keywords

  • 5-hydroxytryptamine
  • Ammonia
  • AVT
  • Cortisol
  • Facilitated diffusion
  • Glutamine
  • Ornithine urea cycle
  • Pavement cells
  • Serotonin
  • UT-A
  • Vesicular trafficking

ASJC Scopus subject areas

  • Biochemistry
  • Physiology

Cite this

Pulsatile urea excretion in the gulf toadfish : Mechanisms and controls. / Wood, Chris M.; Mcdonald, Danielle M; Sundin, Lena; Laurent, Pierre; Walsh, Patrick J.

In: Comparative Biochemistry and Physiology - B Biochemistry and Molecular Biology, Vol. 136, No. 4, 01.12.2003, p. 667-684.

Research output: Contribution to journalArticle

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