Methysergide delays the decompensatory responses to severe hemorrhage by activating 5-HT(1A) receptors

Karie E. Scrogin, Alan Kim Johnson, Virginia Brooks

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19 Citations (Scopus)

Abstract

Central administration of the serotonin receptor ligand methysergide delays the decompensatory response to hypotensive hemorrhage. This study was performed to determine the receptor subtype that mediates this effect. Lateral ventricular (LV) injection of methysergide (40 μg) delayed the hypotensive, bradycardic, and sympathoinhibitory responses to blood withdrawal (1.26 ml/min) in conscious rats. The response was quantified, in part, as the blood volume withdrawal that produced a 40-mmHg fall in blood pressure. The delayed hypotensive response produced by methysergide (8.2 ± 0.2 vs. 5.6 ± 0.2 ml, P <0.01) was reversed by the 5-hydroxytryptamine (HT)(1A) antagonist WAY-100635 (30 μg iv: 6.7 ± 0.4 ml, P <0.01; 100 μg iv: 5.6 ± 0.1 ml, P <0.01). LV injection of the 5-HT(1A) agonist (+)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) also delayed the hypotensive (10 μg: 8.6 ± 0.3, P <0.01; 20 μg: 9.2 ± 0.3 ml, P <0.01), bradycardic, and sympatho-inhibitory responses to hemorrhage. WAY-100635 (10 μg iv) completely reversed the effects of 8-OH-DPAT (20 μg: 5.4 ± 0.3 ml). Neither selective blockade of 5-HT2 receptors nor stimulation of 5-HT(1B/1D) receptors had any effect on hemorrhage responses. These data indicate that methysergide stimulates 5-HT(1A) receptors to delay the decompensatory responses to hemorrhage.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume279
Issue number5 48-5
StatePublished - 2000

Fingerprint

Methysergide
Receptor, Serotonin, 5-HT1A
8-Hydroxy-2-(di-n-propylamino)tetralin
Hemorrhage
Receptor, Serotonin, 5-HT1B
Serotonin Receptor Agonists
Serotonin Antagonists
Injections
Serotonin Receptors
Blood Volume
Blood Pressure
Ligands
hydroxide ion
N-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamide

Keywords

  • Blood pressure
  • Renal sympathetic activity
  • Serotonin

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Methysergide delays the decompensatory responses to severe hemorrhage by activating 5-HT(1A) receptors",
abstract = "Central administration of the serotonin receptor ligand methysergide delays the decompensatory response to hypotensive hemorrhage. This study was performed to determine the receptor subtype that mediates this effect. Lateral ventricular (LV) injection of methysergide (40 μg) delayed the hypotensive, bradycardic, and sympathoinhibitory responses to blood withdrawal (1.26 ml/min) in conscious rats. The response was quantified, in part, as the blood volume withdrawal that produced a 40-mmHg fall in blood pressure. The delayed hypotensive response produced by methysergide (8.2 ± 0.2 vs. 5.6 ± 0.2 ml, P <0.01) was reversed by the 5-hydroxytryptamine (HT)(1A) antagonist WAY-100635 (30 μg iv: 6.7 ± 0.4 ml, P <0.01; 100 μg iv: 5.6 ± 0.1 ml, P <0.01). LV injection of the 5-HT(1A) agonist (+)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) also delayed the hypotensive (10 μg: 8.6 ± 0.3, P <0.01; 20 μg: 9.2 ± 0.3 ml, P <0.01), bradycardic, and sympatho-inhibitory responses to hemorrhage. WAY-100635 (10 μg iv) completely reversed the effects of 8-OH-DPAT (20 μg: 5.4 ± 0.3 ml). Neither selective blockade of 5-HT2 receptors nor stimulation of 5-HT(1B/1D) receptors had any effect on hemorrhage responses. These data indicate that methysergide stimulates 5-HT(1A) receptors to delay the decompensatory responses to hemorrhage.",
keywords = "Blood pressure, Renal sympathetic activity, Serotonin",
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T1 - Methysergide delays the decompensatory responses to severe hemorrhage by activating 5-HT(1A) receptors

AU - Scrogin, Karie E.

AU - Johnson, Alan Kim

AU - Brooks, Virginia

PY - 2000

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N2 - Central administration of the serotonin receptor ligand methysergide delays the decompensatory response to hypotensive hemorrhage. This study was performed to determine the receptor subtype that mediates this effect. Lateral ventricular (LV) injection of methysergide (40 μg) delayed the hypotensive, bradycardic, and sympathoinhibitory responses to blood withdrawal (1.26 ml/min) in conscious rats. The response was quantified, in part, as the blood volume withdrawal that produced a 40-mmHg fall in blood pressure. The delayed hypotensive response produced by methysergide (8.2 ± 0.2 vs. 5.6 ± 0.2 ml, P <0.01) was reversed by the 5-hydroxytryptamine (HT)(1A) antagonist WAY-100635 (30 μg iv: 6.7 ± 0.4 ml, P <0.01; 100 μg iv: 5.6 ± 0.1 ml, P <0.01). LV injection of the 5-HT(1A) agonist (+)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) also delayed the hypotensive (10 μg: 8.6 ± 0.3, P <0.01; 20 μg: 9.2 ± 0.3 ml, P <0.01), bradycardic, and sympatho-inhibitory responses to hemorrhage. WAY-100635 (10 μg iv) completely reversed the effects of 8-OH-DPAT (20 μg: 5.4 ± 0.3 ml). Neither selective blockade of 5-HT2 receptors nor stimulation of 5-HT(1B/1D) receptors had any effect on hemorrhage responses. These data indicate that methysergide stimulates 5-HT(1A) receptors to delay the decompensatory responses to hemorrhage.

AB - Central administration of the serotonin receptor ligand methysergide delays the decompensatory response to hypotensive hemorrhage. This study was performed to determine the receptor subtype that mediates this effect. Lateral ventricular (LV) injection of methysergide (40 μg) delayed the hypotensive, bradycardic, and sympathoinhibitory responses to blood withdrawal (1.26 ml/min) in conscious rats. The response was quantified, in part, as the blood volume withdrawal that produced a 40-mmHg fall in blood pressure. The delayed hypotensive response produced by methysergide (8.2 ± 0.2 vs. 5.6 ± 0.2 ml, P <0.01) was reversed by the 5-hydroxytryptamine (HT)(1A) antagonist WAY-100635 (30 μg iv: 6.7 ± 0.4 ml, P <0.01; 100 μg iv: 5.6 ± 0.1 ml, P <0.01). LV injection of the 5-HT(1A) agonist (+)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) also delayed the hypotensive (10 μg: 8.6 ± 0.3, P <0.01; 20 μg: 9.2 ± 0.3 ml, P <0.01), bradycardic, and sympatho-inhibitory responses to hemorrhage. WAY-100635 (10 μg iv) completely reversed the effects of 8-OH-DPAT (20 μg: 5.4 ± 0.3 ml). Neither selective blockade of 5-HT2 receptors nor stimulation of 5-HT(1B/1D) receptors had any effect on hemorrhage responses. These data indicate that methysergide stimulates 5-HT(1A) receptors to delay the decompensatory responses to hemorrhage.

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