Dogmas and controversies in the handling of nitrogenous wastes: 5-HT 2-like receptors are involved in triggering pulsatile urea excretion in the gulf toadfish, Opsanus beta

Danielle M Mcdonald, Patrick J. Walsh

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

When injected arterially, serotonin (5-hydroxytryptamine; 5-HT) has been shown to elicit naturally sized urea pulse events in the gulf toadfish, Opsanus beta. The goal of the present study was to determine which 5-HT receptor(s) was involved in mediating this serotonergic stimulation of the pulsatile excretion mechanism. Toadfish were surgically implanted with caudal arterial catheters and intraperitoneal catheters and injected with either 8-OH-DPAT (1 μmol kg -1), a selective 5-HT1A receptor agonist, α-methyl-5-HT (1 μmol kg-1), a 5-HT2 receptor agonist, or ketanserin, a 5-HT2 receptor antagonist (0.01, 0.1, 1 and 10 μmol kg-1) plus α-methyl-5-HT. 8-OH-DPAT injection did not mediate an increase in urea excretion, ruling out the involvement of 5-HT1A receptors in pulsatile excretion. However, within 5 min, α-methyl-5-HT injection caused an increase in the excretion of urea in >95% (N=2T) of the fish injected, with an average pulse size of 652±102 μmol N kg-1 (N=26). With α-methyl-5-HT injection there was no corresponding increase in ammonia or [3H]PEG 4000 permeability. Urea pulses elicited by α-methyl-5-HT were inhibited in a dose-dependent fashion by the 5-HT2 receptor antagonist ketanserin, which at low doses caused a significant inhibition of pulse size and at higher doses significantly inhibited the occurrence of pulsatile excretion altogether. However, neither 8-OH-DPAT nor α-methyl 5-HT injection had an effect on plasma cortisol or plasma urea concentrations. These findings suggest the involvement of a 5-HT2-like receptor in the regulation of pulsatile urea excretion.

Original languageEnglish
Pages (from-to)2003-2010
Number of pages8
JournalJournal of Experimental Biology
Volume207
Issue number12
DOIs
StatePublished - May 1 2004

Fingerprint

Batrachoidiformes
Serotonin 5-HT2 Receptors
serotonin
excretion
urea
Urea
Serotonin
receptors
8-Hydroxy-2-(di-n-propylamino)tetralin
injection
Serotonin 5-HT2 Receptor Antagonists
Ketanserin
Injections
Receptor, Serotonin, 5-HT1A
plasma
catheters
agonists
antagonists
Catheters
dosage

Keywords

  • α-methyl-5-HT
  • 8-OH-DPAT
  • Ketanserin
  • Serotonin
  • Serotonin receptor

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Agricultural and Biological Sciences (miscellaneous)

Cite this

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title = "Dogmas and controversies in the handling of nitrogenous wastes: 5-HT 2-like receptors are involved in triggering pulsatile urea excretion in the gulf toadfish, Opsanus beta",
abstract = "When injected arterially, serotonin (5-hydroxytryptamine; 5-HT) has been shown to elicit naturally sized urea pulse events in the gulf toadfish, Opsanus beta. The goal of the present study was to determine which 5-HT receptor(s) was involved in mediating this serotonergic stimulation of the pulsatile excretion mechanism. Toadfish were surgically implanted with caudal arterial catheters and intraperitoneal catheters and injected with either 8-OH-DPAT (1 μmol kg -1), a selective 5-HT1A receptor agonist, α-methyl-5-HT (1 μmol kg-1), a 5-HT2 receptor agonist, or ketanserin, a 5-HT2 receptor antagonist (0.01, 0.1, 1 and 10 μmol kg-1) plus α-methyl-5-HT. 8-OH-DPAT injection did not mediate an increase in urea excretion, ruling out the involvement of 5-HT1A receptors in pulsatile excretion. However, within 5 min, α-methyl-5-HT injection caused an increase in the excretion of urea in >95{\%} (N=2T) of the fish injected, with an average pulse size of 652±102 μmol N kg-1 (N=26). With α-methyl-5-HT injection there was no corresponding increase in ammonia or [3H]PEG 4000 permeability. Urea pulses elicited by α-methyl-5-HT were inhibited in a dose-dependent fashion by the 5-HT2 receptor antagonist ketanserin, which at low doses caused a significant inhibition of pulse size and at higher doses significantly inhibited the occurrence of pulsatile excretion altogether. However, neither 8-OH-DPAT nor α-methyl 5-HT injection had an effect on plasma cortisol or plasma urea concentrations. These findings suggest the involvement of a 5-HT2-like receptor in the regulation of pulsatile urea excretion.",
keywords = "α-methyl-5-HT, 8-OH-DPAT, Ketanserin, Serotonin, Serotonin receptor",
author = "Mcdonald, {Danielle M} and Walsh, {Patrick J.}",
year = "2004",
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T2 - 5-HT 2-like receptors are involved in triggering pulsatile urea excretion in the gulf toadfish, Opsanus beta

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AU - Walsh, Patrick J.

PY - 2004/5/1

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N2 - When injected arterially, serotonin (5-hydroxytryptamine; 5-HT) has been shown to elicit naturally sized urea pulse events in the gulf toadfish, Opsanus beta. The goal of the present study was to determine which 5-HT receptor(s) was involved in mediating this serotonergic stimulation of the pulsatile excretion mechanism. Toadfish were surgically implanted with caudal arterial catheters and intraperitoneal catheters and injected with either 8-OH-DPAT (1 μmol kg -1), a selective 5-HT1A receptor agonist, α-methyl-5-HT (1 μmol kg-1), a 5-HT2 receptor agonist, or ketanserin, a 5-HT2 receptor antagonist (0.01, 0.1, 1 and 10 μmol kg-1) plus α-methyl-5-HT. 8-OH-DPAT injection did not mediate an increase in urea excretion, ruling out the involvement of 5-HT1A receptors in pulsatile excretion. However, within 5 min, α-methyl-5-HT injection caused an increase in the excretion of urea in >95% (N=2T) of the fish injected, with an average pulse size of 652±102 μmol N kg-1 (N=26). With α-methyl-5-HT injection there was no corresponding increase in ammonia or [3H]PEG 4000 permeability. Urea pulses elicited by α-methyl-5-HT were inhibited in a dose-dependent fashion by the 5-HT2 receptor antagonist ketanserin, which at low doses caused a significant inhibition of pulse size and at higher doses significantly inhibited the occurrence of pulsatile excretion altogether. However, neither 8-OH-DPAT nor α-methyl 5-HT injection had an effect on plasma cortisol or plasma urea concentrations. These findings suggest the involvement of a 5-HT2-like receptor in the regulation of pulsatile urea excretion.

AB - When injected arterially, serotonin (5-hydroxytryptamine; 5-HT) has been shown to elicit naturally sized urea pulse events in the gulf toadfish, Opsanus beta. The goal of the present study was to determine which 5-HT receptor(s) was involved in mediating this serotonergic stimulation of the pulsatile excretion mechanism. Toadfish were surgically implanted with caudal arterial catheters and intraperitoneal catheters and injected with either 8-OH-DPAT (1 μmol kg -1), a selective 5-HT1A receptor agonist, α-methyl-5-HT (1 μmol kg-1), a 5-HT2 receptor agonist, or ketanserin, a 5-HT2 receptor antagonist (0.01, 0.1, 1 and 10 μmol kg-1) plus α-methyl-5-HT. 8-OH-DPAT injection did not mediate an increase in urea excretion, ruling out the involvement of 5-HT1A receptors in pulsatile excretion. However, within 5 min, α-methyl-5-HT injection caused an increase in the excretion of urea in >95% (N=2T) of the fish injected, with an average pulse size of 652±102 μmol N kg-1 (N=26). With α-methyl-5-HT injection there was no corresponding increase in ammonia or [3H]PEG 4000 permeability. Urea pulses elicited by α-methyl-5-HT were inhibited in a dose-dependent fashion by the 5-HT2 receptor antagonist ketanserin, which at low doses caused a significant inhibition of pulse size and at higher doses significantly inhibited the occurrence of pulsatile excretion altogether. However, neither 8-OH-DPAT nor α-methyl 5-HT injection had an effect on plasma cortisol or plasma urea concentrations. These findings suggest the involvement of a 5-HT2-like receptor in the regulation of pulsatile urea excretion.

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