Inhibitory presynaptic 5-hydroxytryptamine (5-HT) receptors on the sympathetic nerves of the human saphenous vein

Göthert, M.; Kollecker, P.; Rohm, N; Zerkowski, Hans‐Reinhard

doi:10.1007/bf00500081

Cited by 39 publications

(7 citation statements)

References 28 publications

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“…Ketanserin in the concentration used (0.1 tIM) probably did not act on pre-or postjunctional a-receptors, since it did not affect the tritium efflux or the contraction of the preparation induced by neurogenic stimulation. This is consistent with the findings of Gothert et al (1986) for the human saphenous vein.…”

Section: Recording Of Tritium Releasesupporting

confidence: 93%

Characterization of presynaptic 5‐HT receptors on adrenergic nerves supplying the bovine ovarian follicle

Kannisto

Owman

Schmidt

et al. 1987

British J Pharmacology

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1 The effects of 5-hydroxytryptamine (5-HT) on contraction and release of [3H]-noradrenaline were investigated in vitro in bovine ovarian follicle strips. Using available selective agonists and antagonists, an effort was made to characterize the type of receptor mediating the inhibitory effect of 5-HT on neurogenic contraction and release of [3H]-noradrenaline by electrical field stimulation. 2 5-Hydroxytryptamine inhibited the neurogenic contraction and release of [3H]-noradrenaline evoked by electrical field stimulation in a concentration-dependent manner. Like 5-HT, 5-carboxamidotryptamine (5-CT) and methysergide reduced the transmitter release as well as the neurogenic contraction, whereas 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) failed to inhibit both responses in concentrations up to 0.1 LM.3 The 5-HT (1 gM)-induced inhibition of contractile responses was more evident during stimulation at low frequencies (4 and 8 Hz) than during high frequency electrical stimulation (16 and 32 Hz). 4 Methiothepin (1 jM) and methysergide (10 jM) significantly antagonized the inhibitory effect of 5-HT on the electrically evoked release of tritium, whereas cyanopindolol, MDL 72222 and ketanserin (all 0.1I M) were without effect. In addition, ketanserin, MDL 72222, cimetidine, pyrilamine, atropine, propranolol and indomethacin were without effect on the 5-HT-induced inhibition of the neurogenic contraction. 5 It is suggested that 5-HT inhibits the electrically evoked transmitter release from adrenergic nerves in the bovine ovarian follicle wall via prejunctional 5-HT,-like receptors. This was based on the findings that 5-CT was a potent agonist, methiothepin an antagonist and the lack of effect of MDL 72222, cyanopindolol and ketanserin.

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Section: Recording Of Tritium Releasesupporting

confidence: 93%

Characterization of presynaptic 5‐HT receptors on adrenergic nerves supplying the bovine ovarian follicle

Kannisto

Owman

Schmidt

et al. 1987

British J Pharmacology

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“…In particular, inhibitory presynaptic 5-HT 1B/1D receptors have been identified on the noradrenergic axon terminals of the cardiovascular system of various species both in vitro and in vivo (Charlton et al, 1986;Göthert et al, 1986;Molderings et al, 1987Molderings et al, , 1990Molderings et al, , 1996Medhurst et al, 1997;Morá n et al, 1998;Harris et al, 2002). Therefore, one could expect that the noradrenergic nerve terminals in the CNS might also be endowed with inhibitory presynaptic 5-HT 1B/1D receptors.…”

Section: A General Aspectsmentioning

confidence: 99%

5-HT Receptor Regulation of Neurotransmitter Release

Fink¹,

Göthert²

2007

Pharmacol Rev

323

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“…On the basis of the results obtained in the human saphenous vein (see Introduction; G6thert et al 1986;), our working hypothesis was that the inhibitory presynaptic 5-HT receptors in the human atrium Table 4 Comparison of the potencies of 5-HT receptor agonists in inhibiting electrically evoked tritium overflow from strips of human atrial appendages (pICs0 values from Table 2) with their affinities (pKi) reported in the literature for various cloned or native 5-HT receptors (references in parentheses). Each regression analysis is based on the comparison of the potencies and affinities of 5 to 7 compounds.…”

Section: Classification Of Presynaptic 5-ht Receptorsmentioning

confidence: 99%

Inhibition of noradrenaline release via presynaptic 5-HT1Da receptors in human atrium

Frölich

Likungu

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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In segments of human right atrial appendages preincubated with [3H]noradrenaline and superfused with physiological salt solution containing desipramine and corticosterone, we determined the effects of 5-hydroxytryptamine (5-HT) receptor agonists and antagonists on tritium overflow evoked by transmural electrical stimulation (2 Hz). Tritium overflow was inhibited by 5-HT, 5-carboxamidotryptamine (5-CT), 5-methoxytryptamine (5-MeOT), 5-methoxy-3(1,2,3,6-tetrahydro-4-pyridinyl)-1H indole succinate (RU 24969) and sumatriptan. Yohimbine and oxymetazoline (in the presence of idazoxan) also inhibited tritium overflow. The inhibitory potency of the drugs was significantly correlated with their affinity for 5-HTID receptors in human brain and for cloned human 5-HT1D alpha and 5-HT1D beta receptors, but not with their affinity for 5-HT1B, 5-HT1E, 5-HT1F, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3, 5-HT5A, 5-HT5B and 5-HT7 receptors. The potency order 5-CT > 5-HT > 5-MeOT is opposite to the order of affinities reported for 5-HT6 binding sites. The preferential 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetraline (up to 0.3 microM) and the selective 5-HT4 receptor agonist cisapride (up to 1 microM) failed to inhibit tritium overflow. L-694,247, a potent 5-HT1D beta receptor agonist, did not inhibit tritium overflow, but counteracted the inhibitory effect of 5-HT. Ketanserin at a concentration which should block 5-HT1D alpha but not 5-HT1D beta receptors and methiothepin at a concentration which may be assumed to block both 5-HT1D alpha and 5-HT1D beta receptors antagonized the inhibitory effect of 5-HT. Propranolol and ondansetron did not modify the 5-HT-induced inhibition of release. In conclusion, noradrenaline release in human right atrial appendages is inhibited via 5-HT receptors which are located on the noradrenergic axon terminals. These inhibitory presynaptic 5-HT receptors belong to the 5-HT1D subfamily. The ability of ketanserin to antagonize the inhibitory effect induced by activation of these receptors suggests that they can be subclassified as 5-HT1D alpha.

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Inhibitory presynaptic 5-hydroxytryptamine (5-HT) receptors on the sympathetic nerves of the human saphenous vein

Cited by 39 publications

References 28 publications

Characterization of presynaptic 5‐HT receptors on adrenergic nerves supplying the bovine ovarian follicle

Characterization of presynaptic 5‐HT receptors on adrenergic nerves supplying the bovine ovarian follicle

5-HT Receptor Regulation of Neurotransmitter Release

Inhibition of noradrenaline release via presynaptic 5-HT1Da receptors in human atrium

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