Effect of 5-hydroxytryptamine on neurogenic vasoconstriction in the isolated, autoperfused hindquarters of the rat

Authors: Calama, E1; Ortíz de Urbina, AV1; Morán, A1; Martín, ML1; San Román, L1

Source: Clinical and Experimental Pharmacology and Physiology, Volume 32, Number 10, October 2005 , pp. 894-900(7)

Publisher: Blackwell Publishing

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Abstract:

SUMMARY

1. In the present study, we analysed the effect of different doses of 5-hydroxytryptamine (5-HT; intravenous infusions of 0.001–40 µg/kg per min) in the autoperfused hindquarters of the rat subjected to electrical stimulation (frequencies of 0.5–20 Hz) of the lumbar chains, investigating the relationship between the adrenergic and serotonergic systems in this vascular bed.

2. Because we observed that 5-HT inhibited the increases in perfusion pressure induced by electrical stimulation of the lumbar chains, we used different agonists and antagonists to analyse the mechanism of action of 5-HT.

3. The effect of 5-HT was inhibited by methiothepin (a non-specific 5-HT receptor antagonist), but not by ritanserin (a selective 5-HT2 receptor antagonist). The effects of 5-HT were mimicked by 5-carboxamidotryptamine (a 5-HT1 receptor agonist) and L-694 247 (a selective 5-HT1D receptor agonist), but not by 8-hydroxy-2-dipropylaminotetralin (a 5-HT1A receptor agonist), CGS-12066B (a 5-HT1B receptor agonist), agr-methyl-5-HT (a 5-HT2 receptor agonist), 1-(3-chlorophenyl) piperazine (a 5-HT2C receptor agonist) or 1-phenylbiguanide (a 5-HT3 receptor agonist). The selective 5-HT1D/1B receptor antagonist BRL 15572 inhibited the effect of the agonist L-694 247.

4. Our data suggest that 5-HT inhibits the increases in perfusion pressure induced by the electrical stimulation of the lumbar chains, acting on presynaptic 5-HT1D receptors and decreasing the release of noradrenaline from the sympathetic nerves in the hindquarter vascular bed of the rat.

Keywords: electrical stimulation; hindquarter vascular bed; 5-HT1D receptors; 5-hydroxytryptamine; lumbar chains; serotonin

Document Type: Original article

DOI: 10.1111/j.1440-1681.2010.04281.x

Affiliations: 1: Laboratorio de Farmacognosia y Farmacología, Departamento de Fisiología y Farmacología, Facultad de Farmacia, Universidad de Salamanca, Campus Miguel de Unamuno, Salamanca, Spain

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