Literature DB >> 9318847

Pulsatile urea excretion in the toadfish (Opsanus beta) is due to a pulsatile excretion mechanism, not a pulsatile production mechanism

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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.

Entities:  

Year:  1997        PMID: 9318847     DOI: 10.1242/jeb.200.6.1039

Source DB:  PubMed          Journal:  J Exp Biol        ISSN: 0022-0949            Impact factor:   3.312


  9 in total

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Authors:  Rasmus Ern; Andrew J Esbaugh
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2.  Respiratory plasticity is insufficient to alleviate blood acid-base disturbances after acclimation to ocean acidification in the estuarine red drum, Sciaenops ocellatus.

Authors:  Andrew J Esbaugh; Rasmus Ern; Wiolene M Nordi; Abbey S Johnson
Journal:  J Comp Physiol B       Date:  2016-01       Impact factor: 2.200

Review 3.  The physiology and evolution of urea transport in fishes.

Authors:  M D McDonald; C P Smith; P J Walsh
Journal:  J Membr Biol       Date:  2007-01-30       Impact factor: 1.843

4.  Glucocorticoid receptors are involved in the regulation of pulsatile urea excretion in toadfish.

Authors:  M D McDonald; C M Wood; M Grosell; P J Walsh
Journal:  J Comp Physiol B       Date:  2004-10-28       Impact factor: 2.200

5.  A critical analysis of transepithelial potential in intact killifish (Fundulus heteroclitus) subjected to acute and chronic changes in salinity.

Authors:  Chris M Wood; Martin Grosell
Journal:  J Comp Physiol B       Date:  2008-04-01       Impact factor: 2.200

6.  Impacts of ocean acidification on respiratory gas exchange and acid-base balance in a marine teleost, Opsanus beta.

Authors:  Andrew J Esbaugh; Rachael Heuer; Martin Grosell
Journal:  J Comp Physiol B       Date:  2012-05-12       Impact factor: 2.200

7.  The effect of chronic cortisol elevation on urea metabolism and excretion in the rainbow trout (Oncorhynchus mykiss).

Authors:  M D McDonald; C M Wood
Journal:  J Comp Physiol B       Date:  2003-10-28       Impact factor: 2.200

8.  Pulsatile urea excretion in Gulf toadfish: the role of circulating serotonin and additional 5-HT receptor subtypes.

Authors:  Maria C Cartolano; Haley N Gancel; Joshua Lonthair; Chris M Wood; M Danielle McDonald
Journal:  J Comp Physiol B       Date:  2019-07-17       Impact factor: 2.200

9.  Treatment with the selective serotonin reuptake inhibitor, fluoxetine, attenuates the fish hypoxia response.

Authors:  Jennifer M Panlilio; Sara Marin; Marissa B Lobl; M Danielle McDonald
Journal:  Sci Rep       Date:  2016-08-08       Impact factor: 4.379

  9 in total

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