5-Hydroxytryptamine initiates pulsatile urea excretion from perfused gills of the gulf toadfish (Opsanus beta)

Danielle M Mcdonald, Patrick J. Walsh, Chris M. Wood

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

When stressed, toadfish become ureotelic and excrete almost all of their nitrogenous waste in 1-3 daily pulses of urea-N across the gills. Intravascular injections of 5-hydroxytyptamine (5-HT; serotonin) and analogues also elicit marked excretory pulses of urea-N from toadfish in vivo, suggesting that 5-HT release is the proximate trigger for spontaneous pulses. However it is unclear whether 5-HT is acting on the gills directly or elsewhere to cause the effect indirectly. A perfused whole gill preparation which maintained normal pressure relationships and stable vascular resistance was employed to address this question. Bolus injections into the ventral aortic perfusate of either 5-HT (1, 10μmolkg-1) or the specific 5-HT2 receptor agonist α-methyl 5-HT (1, 10μmolkg-1) elicited rapid urea-N pulses from perfused toadfish gills. The effective doses, the post-injection delays (5.5±1.3min, range=2-22), the percent occurrences (57-85%), and the magnitude of the induced urea-N pulses (615.4±131.3μmol-Nkg-1, range 66.0-2634.0), were all similar to those previously reported when these agents were injected in vivo. Bolus injections of 5-HT and α-methyl 5-HT also elicited a biphasic response in ventral aortic pressure, reflecting an initial rapid short-lived vasodilation and a subsequent longer-lasting vasoconstriction. These events were similar to those which have been recorded to occur at a greater frequency during spontaneous urea-N pulsing in vivo. Neither the urea-N pulsing nor the cardiovascular responses to 5-HT were inhibited by the 5-HT2A receptor subtype blocker, ketanserin (pre-injection with 10μmolkg-1 plus 33μmolL-1 in the perfusate). Overall, these results provide strong support for the idea that the proximate stimulus for natural urea pulsing in vivo is 5-HT mobilization, acting directly in the gills.

Original languageEnglish
Pages (from-to)30-37
Number of pages8
JournalComparative Biochemistry and Physiology - A Molecular and Integrative Physiology
Volume163
Issue number1
DOIs
StatePublished - Sep 1 2012

Fingerprint

Batrachoidiformes
Urea
Serotonin
Injections
Serotonin 5-HT2 Receptor Agonists
Receptor, Serotonin, 5-HT2A
Ketanserin
Vasoconstriction
Vasodilation
Vascular Resistance
Arterial Pressure

Keywords

  • α-Methyl 5-HT
  • 5-HT
  • Blood pressure
  • Ketanserin
  • Serotonin
  • Urea transporter
  • Vascular resistance

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Physiology

Cite this

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title = "5-Hydroxytryptamine initiates pulsatile urea excretion from perfused gills of the gulf toadfish (Opsanus beta)",
abstract = "When stressed, toadfish become ureotelic and excrete almost all of their nitrogenous waste in 1-3 daily pulses of urea-N across the gills. Intravascular injections of 5-hydroxytyptamine (5-HT; serotonin) and analogues also elicit marked excretory pulses of urea-N from toadfish in vivo, suggesting that 5-HT release is the proximate trigger for spontaneous pulses. However it is unclear whether 5-HT is acting on the gills directly or elsewhere to cause the effect indirectly. A perfused whole gill preparation which maintained normal pressure relationships and stable vascular resistance was employed to address this question. Bolus injections into the ventral aortic perfusate of either 5-HT (1, 10μmolkg-1) or the specific 5-HT2 receptor agonist α-methyl 5-HT (1, 10μmolkg-1) elicited rapid urea-N pulses from perfused toadfish gills. The effective doses, the post-injection delays (5.5±1.3min, range=2-22), the percent occurrences (57-85{\%}), and the magnitude of the induced urea-N pulses (615.4±131.3μmol-Nkg-1, range 66.0-2634.0), were all similar to those previously reported when these agents were injected in vivo. Bolus injections of 5-HT and α-methyl 5-HT also elicited a biphasic response in ventral aortic pressure, reflecting an initial rapid short-lived vasodilation and a subsequent longer-lasting vasoconstriction. These events were similar to those which have been recorded to occur at a greater frequency during spontaneous urea-N pulsing in vivo. Neither the urea-N pulsing nor the cardiovascular responses to 5-HT were inhibited by the 5-HT2A receptor subtype blocker, ketanserin (pre-injection with 10μmolkg-1 plus 33μmolL-1 in the perfusate). Overall, these results provide strong support for the idea that the proximate stimulus for natural urea pulsing in vivo is 5-HT mobilization, acting directly in the gills.",
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T1 - 5-Hydroxytryptamine initiates pulsatile urea excretion from perfused gills of the gulf toadfish (Opsanus beta)

AU - Mcdonald, Danielle M

AU - Walsh, Patrick J.

AU - Wood, Chris M.

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N2 - When stressed, toadfish become ureotelic and excrete almost all of their nitrogenous waste in 1-3 daily pulses of urea-N across the gills. Intravascular injections of 5-hydroxytyptamine (5-HT; serotonin) and analogues also elicit marked excretory pulses of urea-N from toadfish in vivo, suggesting that 5-HT release is the proximate trigger for spontaneous pulses. However it is unclear whether 5-HT is acting on the gills directly or elsewhere to cause the effect indirectly. A perfused whole gill preparation which maintained normal pressure relationships and stable vascular resistance was employed to address this question. Bolus injections into the ventral aortic perfusate of either 5-HT (1, 10μmolkg-1) or the specific 5-HT2 receptor agonist α-methyl 5-HT (1, 10μmolkg-1) elicited rapid urea-N pulses from perfused toadfish gills. The effective doses, the post-injection delays (5.5±1.3min, range=2-22), the percent occurrences (57-85%), and the magnitude of the induced urea-N pulses (615.4±131.3μmol-Nkg-1, range 66.0-2634.0), were all similar to those previously reported when these agents were injected in vivo. Bolus injections of 5-HT and α-methyl 5-HT also elicited a biphasic response in ventral aortic pressure, reflecting an initial rapid short-lived vasodilation and a subsequent longer-lasting vasoconstriction. These events were similar to those which have been recorded to occur at a greater frequency during spontaneous urea-N pulsing in vivo. Neither the urea-N pulsing nor the cardiovascular responses to 5-HT were inhibited by the 5-HT2A receptor subtype blocker, ketanserin (pre-injection with 10μmolkg-1 plus 33μmolL-1 in the perfusate). Overall, these results provide strong support for the idea that the proximate stimulus for natural urea pulsing in vivo is 5-HT mobilization, acting directly in the gills.

AB - When stressed, toadfish become ureotelic and excrete almost all of their nitrogenous waste in 1-3 daily pulses of urea-N across the gills. Intravascular injections of 5-hydroxytyptamine (5-HT; serotonin) and analogues also elicit marked excretory pulses of urea-N from toadfish in vivo, suggesting that 5-HT release is the proximate trigger for spontaneous pulses. However it is unclear whether 5-HT is acting on the gills directly or elsewhere to cause the effect indirectly. A perfused whole gill preparation which maintained normal pressure relationships and stable vascular resistance was employed to address this question. Bolus injections into the ventral aortic perfusate of either 5-HT (1, 10μmolkg-1) or the specific 5-HT2 receptor agonist α-methyl 5-HT (1, 10μmolkg-1) elicited rapid urea-N pulses from perfused toadfish gills. The effective doses, the post-injection delays (5.5±1.3min, range=2-22), the percent occurrences (57-85%), and the magnitude of the induced urea-N pulses (615.4±131.3μmol-Nkg-1, range 66.0-2634.0), were all similar to those previously reported when these agents were injected in vivo. Bolus injections of 5-HT and α-methyl 5-HT also elicited a biphasic response in ventral aortic pressure, reflecting an initial rapid short-lived vasodilation and a subsequent longer-lasting vasoconstriction. These events were similar to those which have been recorded to occur at a greater frequency during spontaneous urea-N pulsing in vivo. Neither the urea-N pulsing nor the cardiovascular responses to 5-HT were inhibited by the 5-HT2A receptor subtype blocker, ketanserin (pre-injection with 10μmolkg-1 plus 33μmolL-1 in the perfusate). Overall, these results provide strong support for the idea that the proximate stimulus for natural urea pulsing in vivo is 5-HT mobilization, acting directly in the gills.

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KW - Blood pressure

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KW - Urea transporter

KW - Vascular resistance

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