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

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Citation

Scrogin KE, Johnson AK, Brooks VL

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

Am J Physiol Regul Integr Comp Physiol. 2000 Nov;279(5):R1776-86.

PubMed ID
11049861 [ View in PubMed
]
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 microg) 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 microg iv: 6.7 +/- 0.4 ml, P < 0. 01; 100 microg 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 microg: 8.6 +/- 0.3, P < 0.01; 20 microg: 9.2 +/- 0.3 ml, P < 0.01), bradycardic, and sympathoinhibitory responses to hemorrhage. WAY-100635 (10 microg iv) completely reversed the effects of 8-OH-DPAT (20 microg: 5.4 +/- 0.3 ml). Neither selective blockade of 5-HT(2) 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.

DrugBank Data that Cites this Article

Drug Targets
DrugTargetKindOrganismPharmacological ActionActions
Methysergide5-hydroxytryptamine receptor 1AProteinHumans
Yes
Agonist
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