Serotonergic Receptor Subtypes and Vascular Reactivity

Nueten, J. M. Van; Leysen, Josée E.; Clerck, Fred De; Vanhoutte, Paul M.

doi:10.1097/00005344-198406004-00003

Cited by 79 publications

(46 citation statements)

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“…28,29 The present findings thus confirm the previous demonstration 30,31 that endothelium-dependent relaxations of coronary arteries with regenerated endothelium that involve the G i protein mediated pathway, in particular those to serotonin, are blunted selectively, whereas the G q protein mediated endotheliumdependent relaxations, such as those in response to bradykinin, remain unchanged (Figure 1). 7,31,32 Previous findings concluded that the decrease in relaxation to serotonin is due mainly to reduced activity rather than absence or reduced levels of G i proteins to induce activation of eNOS. 32 By contrast, the relaxation pathways in the vascular smooth muscle cells are preserved in preparations with regenerated endothelium, as indicated by the lack of differences in the response to detaNONOate (10 −8 to 10 −4 M) and isoproterenol (10 −9 to 10 −5 M) (Figure 2).…”

Section: ■ Results and Discussionmentioning

confidence: 99%

A-FABP and Oxidative Stress Underlie the Impairment of Endothelium-Dependent Relaxations to Serotonin and the Intima-Medial Thickening in the Porcine Coronary Artery with Regenerated Endothelium

Chan

Zhao²,

Liao³

et al. 2012

ACS Chem. Neurosci.

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Experiments were designed to determine the cause of the selective dysfunction of G i proteins, characterized by a reduced endothelium-dependent relaxation to serotonin (5-hydroxytryptamine), in coronary arteries lined with regenerated endothelial cells. Part of the endothelium of the left anterior descending coronary artery of female pigs was removed in vivo to induce regeneration. The animals were treated chronically with vehicle (control), apocynin (antioxidant), or BMS309403 (A-FABP inhibitor) for 28 days before functional examination and histological analysis of segments of coronary arteries with native or regenerated endothelium of the same hearts. Isometric tension was recorded in organ chambers and cumulative concentrationrelaxation curves obtained in response to endothelium-dependent [serotonin (G i protein mediated activation of eNOS) and bradykinin (G q protein mediated activation of eNOS)] and independent [detaNONOate (cGMP-mediated), isoproterenol (cAMP-mediated)] vasodilators. The two inhibitors tested did not acutely affect relaxations of preparations with either native or regenerated endothelium. In the chronically treated groups, however, both apocynin and BMS309403 abolished the reduction in relaxation to serotonin in segments covered with regenerated endothelium and prevented the intima-medial thickening caused by endothelial regeneration, without affecting responses to bradykinin or endothelium-independent agonists (detaNONOate and isoproterenol). Thus, inhibition of either oxidative stress or A-FABP likely prevents both the selective dysfunction of G i protein mediated relaxation to serotonin and the neointimal thickening resulting from endothelial regeneration.

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Section: ■ Results and Discussionmentioning

confidence: 99%

A-FABP and Oxidative Stress Underlie the Impairment of Endothelium-Dependent Relaxations to Serotonin and the Intima-Medial Thickening in the Porcine Coronary Artery with Regenerated Endothelium

Chan

Zhao²,

Liao³

et al. 2012

ACS Chem. Neurosci.

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“…The low level of 5-HT,, receptor RNA found in brain tissue may then be attributed to the blood vessels. By comparison, the 5-HT,, receptor is expressed in the brain and in the periphery [8,35,36]. Additional research will show if this distinction of 5-HTZB as a peripheral and 5-HT,, as a central receptor is valid.…”

Section: Discussionmentioning

confidence: 96%

Cloning and functional characterization of the human 5‐HT_2B serotonin receptor

et al. 1994

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Recently, we have reported the cloning of the rat 5-HT,, receptor cDNA. This receptor is particularly interesting since it may be involved in diseases such as migraine. Here, we describe the isolation of a human 5-HT,, receptor clone from a cDNA library derived from SH-SYSY cells. Although the receptor sequence was only 80% homologous to the rat sequence, the exon-intron distribution was conserved between the two species. In the human body, the receptor mRNA was detected in most peripheral organs. Only low expression levels were found in the brain. After expression in HEK 293 cells, activation of the receptor stimulated the production of phosphatidylinositol. The pharmacology of this functional response correlated well with that of the rodent receptor.

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“…Under different experimental conditions and working with species other than the rat, other authors have obtained results leading them to propose similar effects of 5-HT: inhibiting or potentiating sympathetic actions. The nature, inhibitory or stimulatory, being dependent on the dose of 5-HT or on the level of sympathetic tone (Martinez & Lokhandwala, 1980;Van Nueten et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory 5‐hydroxytryptamine receptors involved in pressor effects obtained by stimulation of sympathetic outflow from spinal cord in pithed rats

Morán

Velasco

Salvador

et al. 1994

British J Pharmacology

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1 A study was made of the effects of 5-hydroxytryptamine (5-HT) on pressor response induced in vivo by electrical stimulation of the sympathetic outflow from the spinal cord of pithed rats. All animals had been pretreated with atropine. Intravenous infusion of 5-hydroxytryptamine at doses of 10 and 20 jig kg-' min-' reduced the pressor effects obtained by electrical stimulation at intervals of 10 min over the 1 h of infusion. 2 This inhibitory action of 5-HT was depressed by cyproheptadine and methiothepin but was not modified by ketanserin or MDL-72222. By contrast, the inhibitory action of 5-HT was lost in pithed rats that had been pretreated with exogenous noradrenaline.3 The 5-HT, receptor agonist 5-carboxamidotryptamine (5-CT) caused an inhibition of the pressor response, whereas the 5-HT3 receptor agonist, 1-phenylbiguanide, produced a variable but significant increase in the pressor response. The 5-HT2 receptor agonist, m-CPP, did not modify the pressor sympathetic response. 4 Our results suggest that 5-hydroxytryptamine interferes with sympathetic neurotransmission by inhibiting pressor effects as a result of stimulation of the complete sympathetic outflow, and that this inhibition is mainly through a presynaptic 5-HT1 mechanism.

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Serotonergic Receptor Subtypes and Vascular Reactivity

Cited by 79 publications

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A-FABP and Oxidative Stress Underlie the Impairment of Endothelium-Dependent Relaxations to Serotonin and the Intima-Medial Thickening in the Porcine Coronary Artery with Regenerated Endothelium

A-FABP and Oxidative Stress Underlie the Impairment of Endothelium-Dependent Relaxations to Serotonin and the Intima-Medial Thickening in the Porcine Coronary Artery with Regenerated Endothelium

Cloning and functional characterization of the human 5‐HT_2B serotonin receptor

Inhibitory 5‐hydroxytryptamine receptors involved in pressor effects obtained by stimulation of sympathetic outflow from spinal cord in pithed rats

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Serotonergic Receptor Subtypes and Vascular Reactivity

Cited by 79 publications

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A-FABP and Oxidative Stress Underlie the Impairment of Endothelium-Dependent Relaxations to Serotonin and the Intima-Medial Thickening in the Porcine Coronary Artery with Regenerated Endothelium

A-FABP and Oxidative Stress Underlie the Impairment of Endothelium-Dependent Relaxations to Serotonin and the Intima-Medial Thickening in the Porcine Coronary Artery with Regenerated Endothelium

Cloning and functional characterization of the human 5‐HT2B serotonin receptor

Inhibitory 5‐hydroxytryptamine receptors involved in pressor effects obtained by stimulation of sympathetic outflow from spinal cord in pithed rats

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Cloning and functional characterization of the human 5‐HT_2B serotonin receptor