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PubMed1994

[Registration of suspected adverse effects by the Bureau Adverse Effects Drugs; research activities in 1993].

In 1993, the Netherlands Centre for Monitoring of Adverse Reactions to Drugs received 1585 reports of suspected adverse reactions. The most important reports concerned myocardial infarction due to sumatriptan, cholestatic hepatitis due to itraconazole, agranulocytosis due to trazodone and bleeding due to fluoxetine and fluvoxamine. Other published reports concerned cholestatic hepatitis due to amoxicillin/clavulanic acid, hair loss due to beta-blockers, muscle necrosis due to diclofenac, bronchospasm, apnoea and cardiac arrest due to dipyridamole perfusion scintigraphy, interaction of fluvoxamine/fluoxetine and coumarins, liver enzyme elevations due to heparin, skin reactions due to Imedeen, deafness due to neomycin, addiction to nicotine chewing gum, atrial fibrillation and skin reactions due to nicotine patches, interaction between oral contraceptives and terbinafine, neonatal problems caused by psychopharmacological agents, parapemphigus caused by sulfasalazine, taste loss due to terbinafine en intracranial bleeding after use of tranylcypromine and beer. Pharmacoepidemiological studies were performed concerning methods for record linkage, the communication process with respect to the acitretin alert and the adverse events due to sumatriptan.

Drug-Related Side Effects and Adverse Reactions↗
PubMed1993

[Headache--what is the current status?].

Clinical and experimental evidence suggest, that migraine reflects a biological disorder of the brain. On the basis of a genetic predisposition, variations in internal rhythms may change the responsiveness towards external trigger factors. During the migraine attack changes occur in the cortical neuronal activity, in cerebral blood flow and in the activity of neuropeptide neurotransmitters such as substance P and calcitonin-gene-related-peptide. The consequence is an aseptic inflammation in the wall of dural arteries. Sumatriptan is a new agent which selectively acts at 5-HT-1D receptors in brain vessels and improves headache and autonomic symptoms in severe migraine attacks. Sumatriptan is also helpful in the treatment of headache attacks in cluster headache. The treatment of chronic tension-type headache requires the combination of tricyclics with behavioral techniques such as relaxation training.

Analgesics↗
PubMed1994

Serotoninergic receptor subtype in coronary artery smooth muscle from young and atherosclerotic rabbit.

In rabbits fed with hypercholesterolemic diet the normal coronary vasodilator response to serotonin is replaced by vasoconstriction sensitive to 5HT2 receptor blockade. These experiments were designed to determine the receptor subtype involved in the contractile response of large isolated coronary arteries (without endothelium) taken from control and atherosclerotic rabbits. In both tissues the agonists' rank potency was 5-carboxamidotryptamine > serotonin (5HT) > sumatriptan > 8-OHDPAT: (+/-)-8-Hydroxydipropylaminotetralin HBr > 2-methylserotonin. In arteries from young rabbits, 5HT and sumatriptan induced contractions which were not influenced by ketanserin up to 3 x 10(-8) M. However, the 5HT2 antagonist at the concentration of 10(-6) M induced a significant rightward shift of the concentration-response curves. The contractions to the two serotoninergic agonists were competitively inhibited by methiothepin. NAN 190, a 5HT1A antagonist, LY 53857, a 5HT1C and 5HT2 antagonist, cyanopindolol, a 5HT1A and 5HT1B antagonist and ICS 205-930, a 5HT3 and 5HT4 antagonist (up to 10(-6) M) did not inhibit the contractile response to 5HT. Rauwolscine (10(-6) M) significantly shifted the concentration-response curves to the two agonists. Very similar results were obtained in coronary arteries from atherosclerotic rabbits. These data demonstrate that in rabbit epicardial coronary artery smooth muscle, the receptor involved in the serotoninergic response is a 5HT1-like subtype, possibly a 5HT1D. In this preparation, under our experimental conditions, there was no evidence for the presence of 5HT2 receptors. The induction of atherosclerosis did not induce significant changes in the serotoninergic response in these large coronary arteries, illustrating the marked heterogeneity between microvasculature and large arteries in the rabbit heart.

Animals↗
PubMed1993

Mouse 5-hydroxytryptamine5A and 5-hydroxytryptamine5B receptors define a new family of serotonin receptors: cloning, functional expression, and chromosomal localization.

Serotonin [5-hydroxytryptamine (5-HT)] is a neuromodulator that mediates a wide range of physiological functions by activating multiple receptors. Using a strategy based on amino acid sequence homology between 5-HT receptors that interact with guanine nucleotide-binding proteins, we have isolated from a mouse brain library a cDNA encoding a new serotonin receptor. Amino acid sequence comparisons revealed that this receptor was a close relative of the previously identified 5-HT5 receptor but was distant from all other 5-HT receptor subtypes; we therefore named it 5-HT5B. When expressed in COS-7 cells, the 5-HT5B receptor displayed a high affinity for the serotonergic radioligand 125I-lysergic acid diethylamide. Its pharmacological profile was distinct from that of all classic 5-HT receptor subtypes. However, the high affinity of the 5-HT5B receptor for 5-carboxamidotryptamine and its low affinity for sumatriptan indicated that it might correspond to recently described 5-HT1D-like binding sites that were labeled with [3H]5-carboxamidotryptamine and insensitive to sumatriptan. In situ hybridization experiments revealed that the 5-HT5B mRNA was expressed predominantly in the habenula and in the CA1 field of the hippocampus. We also determined the chromosomal localization of the 5-HT5A and 5-HT5B genes and of their human counterparts. The 5-HT5A gene colocalized with the mouse mutation reeler and the human mutation holoprosencephaly type 3, which both result in abnormal brain development, raising the possibility that the 5-HT5A receptor plays a role in brain development.

Amino Acid Sequence↗
PubMed1995

Regulation of [3H]5-HT release in raphe, frontal cortex and hippocampus of 5-HT1B knock-out mice.

Regulation of the electrically evoked release of [3H]5-HT was examined in midbrain, frontal cortex and hippocampus preloaded slices obtained from wild-type and 5-HT1B knock-out mice. In the absence of any drug [3H]5-HT released was increased in midbrain and hippocampus but not in frontal cortex slices of [3H]5-HT1B knock out mice. The selective 5-HT1B agonist CP 93129 and the 5-HT1B/1D agonist sumatriptan, inhibited [3H]5-HT release in hippocampus and cortical slices obtained from control mice but had no effect in mutants. In the two projection areas studied, the non-selective 5-HT agonist 5-carboxyamidotryptamine (5-CT) inhibited [3H]5-HT release in both groups of mice, indicating that additional 5-HT receptors, other than 5-HT1B, might be involved in the regulation of [3H]5-HT release from 5-HT terminals. In slices containing midbrain raphe nuclei, CP 93129 had no effect in either group. In contrast, sumatriptan inhibited [3H]5-HT release in controls and mutants. The latter effect was blocked by the 5-HT1D antagonist GR 127935, but not the 5-HT1A antagonist (+)WAY 100135, thus suggesting that a 5-HT1D-like receptor, possibly 5-HT1D alpha, negatively regulates 5-HT release in mouse midbrain raphe nuclei.

Animals↗
PubMed1997

Effects of KB-2796 on plasma extravasation following antidromic trigeminal stimulation in the rat.

We investigated the effects of KB-2796 (1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)piperazine dihydrochloride), a novel calcium channel blocker, on neurogenic inflammation caused by electrical stimulation in the trigeminal ganglion and on cutaneous reactions induced by inflammatory mediators in rats, by measuring plasma extravasation. Neurogenic inflammation was inhibited by pretreatment with capsaicin (25 mg/kg, s.c.) but not indomethacin (10 mg/kg, i.p.), while phosphoramidon (2.5 mg/kg, i.v.) augmented it. KB-2796 (0.1-1 mg/kg, i.v.) significantly inhibited neurogenic inflammation in a dose dependent manner, without affecting histamine-, bradykinin- or substance P-induced cutaneous reactions. Dimetotiazine (0.3 and 1 mg/kg, i.v.), flunarizine (1 mg/kg, i.v.), mepyramine (1 mg/kg, i.v.) and sumatriptan (1 mg/kg, i.v.) significantly inhibited neurogenic inflammation. However, these compounds also showed complete or partial inhibition of histamine-, bradykinin- or substance P-induced reactions. Nifedipine (0.1 mg/kg, i.v.) did not show marked effects on neurogenic inflammation and cutaneous reactions. The present experiments indicate that neurogenic inflammation is presumably mediated not only by neuropeptides released from trigeminal nerve endings but also by secondarily released histamine, and that KB-2796 like sumatriptan may inhibit neurogenic inflammation caused by trigeminal nerve stimulation probably through inhibition of neuropeptide release but its inhibition may be distinct from the calcium blocking action of the 1,4-dihydropyridine type.

Animals↗
PubMed1998

[Correct use of serotonin agonists in migraine: oral or injectable form?].

Sumatriptan and other selective serotonin agonists represent a major breakthrough in acute migraine treatment. These drugs are very efficacious and generally devoided of important side effects, but they are expensive and therefore have to be compared with other, more conventional drugs with established or assumed efficacy. We summarize the pharmacologic characteristics of Sumatriptan and give recommendations about its use in clinical practice.

Administration, Oral↗
PubMed2001

A clinical trial on a plate? The potential of 384-well format solid phase extraction for high-throughput bioanalysis using liquid chromatography/tandem mass spectrometry.

The application of 384-well format solid phase extraction (SPE) for bioanalysis using liquid chromatography/tandem mass spectrometry (LC/MS/MS) is reported and a 384-well SPE method for the 5-HT agonist sumatriptan in human plasma described. Plasma samples were extracted on a prototype low-density polyethylene 384-well SPE block using a packed bed of 5 mg Oasistrade mark HLB. Liquid handling was automated by a combination of a robotic sampler processor and a 96/384 multi-channel dispensing station. Samples and SPE reagents were drawn through the SPE block by centrifugation. The extracts were analysed by LC/MS/MS with thermally and pneumatically assisted electrospray ionisation and selected reaction monitoring. The method is used to illustrate and discuss the feasibility and viability of sample preparation techniques in high-density microtitre plate format for routine bioanalysis.

Blood Chemical Analysis↗
PubMed2001

Evidence for postjunctional serotonin (5-HT1) receptors in the trigeminocervical complex.

Units linked to stimulation of the superior sagittal sinus were identified and recorded from in the trigeminocervical complex of the anesthetized cat. Iontophoresis of glutamate NMDA receptor agonists increased the baseline-firing rate of these neurons. Coejection of sumatriptan, 4991W93, or ergometrine resulted in a significant reduction in NMDA agonist-induced increases in firing. These data establish the existence of triptan-sensitive (5-HT1) receptors on postsynaptic central trigeminal neurones.

Animals↗
PubMed1993

Therapeutic advances in migraine.

Migraine is a common and debilitating disorder of uncertain pathogenesis. Recent research into the pathophysiology of migraine and serotonin receptors has revolutionized the approach to pharmacotherapy. New medications, such as sumatriptan, and new dosage forms of older medications, including dihydroergotamine, NSAIDs, and phenothiazines are available to treat acute attacks. New prophylactic approaches include the use of calcium-channel blockers, NSAIDs, fluoxetine, and valproate. The addition of several new agents for the acute and prophylactic therapy of migraine has improved the outlook for this disabling disorder.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Neurogenic inflammation in the context of migraine.

Despite considerable research into the pathogenesis of idiopathic headaches, such as migraine, the pathophysiological mechanisms underlying them remain poorly understood. Although it is well established that the trigeminal nerve becomes activated during migraine, the consequences of this activation remain controversial. One theory, based on preclinical observations, is that activation of trigeminal sensory fibers leads to a painful neurogenic inflammation within the meningeal (dural) vasculature mediated by neuropeptide release from trigeminal sensory fibres and characterized by plasma protein extravasation, vasodilation, and mast cell degranulation. Effective antimigraine agents such as ergots, triptans, opioids, and valproate inhibit preclinical neurogenic dural extravasation, suggesting that this activity may be a predictor of potential clinical efficacy of novel agents. However, several clinical trials with other agents that inhibit this process preclinically have failed to show efficacy in the acute treatment of migraine in man. Alternatively, it has been proposed that painful neurogenic vasodilation of meningeal blood vessels could be a key component of the inflammatory process during migraine headache. This view is supported by the observation that jugular plasma levels of the potent vasodilator, calcitonin gene-related peptide (CGRP) are elevated during the headache and normalized by successful sumatriptan treatment. Preclinically, activation of trigeminal sensory fibers evokes a CGRP-mediated neurogenic dural vasodilation, which is blocked by dihydroergotamine, triptans, and opioids but unaffected by NK1 receptor antagonists that failed in clinical trials. These observations suggest that CGRP release with associated neurogenic dural vasodilation may be important in the generation of migraine pain, a theory that would ultimately be tested by the clinical testing of a CGRP receptor antagonist.

Animals↗
PubMed2001

Functional immunohistochemistry of neuropeptides and nitric oxide synthase in the nerve fibers of the supratentorial dura mater in an experimental migraine model.

The supratentorial cerebral dura of the albino rat is equipped with a rich sensory innervation both in the connective tissue and around blood vessels, which includes nociceptive axons and their terminals; these display intense calcitonin gene-related peptide (CGRP) immunoreactivity. Stereotactic electrical stimulation of the trigeminal (Gasserian) ganglion, regarded as an experimental migraine model, caused marked increase and disintegration of club-like perivascular CGRP-immunopositive nerve endings in the dura mater and induced an apparent increase in the lengths of CGRP-immunoreactive axons. Intravenous administration of sumatriptan or eletriptan, prior to electrical stimulation, prevented disintegration of perivascular terminals and induced accumulation of CGRP in terminal and preterminal portions of peripheral sensory axons. Consequently, immunopositive terminals and varicosities increased in size; accumulation of axoplasmic organelles resulted in the "hollow" appearence of numerous varicosities. Since triptans exert their anti-migraine effect by virtue of agonist action on 5-HT(1D/B) receptors, we suggest that these drugs prevent the release of CGRP from perivascular nerve terminals in the dura mater by an action at 5-HT(1D/B) receptors. Nitroglycerine (NitroPOHL), given subcutaneously to rats, induces increased beading of nitric oxide synthase (NOS)-immunoreactive nerve fibers in the supratentorial cerebral dura mater, and an apparent increase in the number of NOS-immunoreactive nerve fibers in the dural areas supplied by the anterior and middle meningeal arteries, and the sinus sagittalis superior. Structural alterations of nitroxidergic axons innervating blood vessels of the dura mater support the idea that nitric oxide (NO) is involved in the induction of headache, a well-known side effect of coronary dilator agents.

Animals↗
PubMed2001

HT29-MTX and Caco-2/TC7 monolayers as predictive models for human intestinal absorption: role of the mucus layer.

The permeability of 19 compounds in both the Caco-2/TC7 and HT29-MTX models was determined, and the ability of each model to predict intestinal absorption in humans was compared. Similar apparent permeability values (log P(app)) were obtained in both models for the majority of compounds tested, and plots of log P(app) versus fraction absorbed in humans gave comparable sigmoidal curves. A linear correlation was also observed between the log P(app) values derived from these two models, which suggests that HT29-MTX is an alternative model for absorption prediction in humans. The similarity of both the diffusion coefficients and permeability values obtained for a range of hydrophilic and lipophilic compounds in the two models indicates that the mucus layer secreted by the human adenocarcinoma HT29-MTX goblet cells does not constitute a diffusion barrier to such compounds. The lack of P-glycoprotein (P-gp) in the HT29-MTX cell line may explain the higher permeability values obtained for cimetidine and sumatriptan in this model compared with those derived from the Caco-2/TC7 monolayers. The results suggest that the HT29-MTX model can be used to rank order the passive permeability of compounds, irrespective of their potential interaction with P-gp, which may facilitate optimization of the physicochemical features of compounds within a chemical series.

Administration, Oral↗
PubMed1993

Cell-specific coupling of the cloned human 5-HT1F receptor to multiple signal transduction pathways.

We recently described the cloning of a fifth member of the 5-hydroxytryptamine (5-HT)1 (serotonin1) receptor class that inhibits adenylyl cyclase, namely the human 5-HT1F receptor (Adham et al. 1993a). In the present study we have examined in greater detail the functional coupling of the 5-HT1F receptor in two different cell lines, NIH-3T3 and LM(tk-) fibroblasts (receptor densities of 1.7 and 4.4 pmol/mg protein, respectively). The maximal inhibitory response elicited by 5-HT was significantly greater in NIH-3T3 as compared to LM(tk-) cells, whereas the EC50 values were comparable. To investigate the relationship between receptor occupancy and inhibition of cAMP accumulation mediated by 5-HT1F receptors in NIH-3T3 cells (and hence the degree of receptor reserve), we used the irreversible receptor antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ). The half-maximal response required only about 10% receptor occupancy, consistent with a receptor reserve of 90% (88 +/- 2.1%, n = 4) for 5-HT-induced inhibition of FSCA. Despite the presence of such a high degree of receptor reserve, a range of intrinsic activities was displayed by structurally diverse classes of compounds. For example, sumatriptan and lysergol were as efficacious as 5-HT itself and thus acted as full agonists, whereas metergoline and 1-NP behaved as partial agonists and as shown previously (Adham et al. 1993a), methiothepin was a silent antagonist (Kb = 438 nM). We have also investigated activation of additional signal transduction pathways by the 5-HT1F receptor and found that the responses differ in the two cell lines with respect to stimulation of phospholipase C. For example, in NIH-3T3 cells no elevation of inositol phosphates (IP) of [Ca2+]i was observed even at very high agonist concentrations (100 microM). In contrast, in LM(tk-) cells concentrations of 5-HT as low as 10 nM induced stimulation of IP and a rapid increase of [Ca2+]i. The 5-HT1F receptor failed to alter arachidonic acid release in either cell line. The maximal increase in IP accumulation in LM(tk-) cells was modest, averaging about 100% above basal. The increases of IP and [Ca2+]i required 5-HT concentrations less than one order of magnitude greater than those inhibiting FSCA (EC50 = 17, 55 and 8 nM, respectively), and both responses were blocked by 100 microM methiothepin. All three responses (cAMP, IP, and [Ca2+]i) were sensitive to pertussis toxin pre-treatment, suggesting the involvement of Gi/Go protein(s) in these signal transduction pathways.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMed1995

5-Hydroxytryptamine 5-HT1D receptors mediating inhibition of cyclic AMP accumulation in Madin-Darby canine kidney (MDCK) cells.

5-Hydroxytryptamine 5-HT1B/5-HT1D receptors are members of the same receptor subfamily, but display a different pharmacology (Hartig et al. (1992) Trends Pharmacol Sci 13: 152-159). Whereas several cell lines have been reported to contain 5-HT1B receptors, none has been described, however, that endogenously expresses well-characterized 5-HT1D receptors. The present study deals with the identification of 5-HT1D receptors inhibiting cyclic AMP accumulation in Madin-Darby canine kidney (MDCK) cells. 5-HT (1 nM-10 microM) induced a concentration-dependent inhibition of the cyclic AMP accumulation stimulated by prostaglandin E1 (1 microM) in MDCK cells. The maximal effect of 5-HT averaged 50% inhibition and was abolished after a pre-treatment of the cells with pertussis toxin. Other agonists mimicked the effects of 5-HT, with the following rank order of potency (pEC50 +/- SEM, n > or = 3): 5-carboxamidotryptamine (8.36 +/- 0.48) > PAPP (p-aminophenylethyl-m-trifluoromethylphenyl piperazine. 7.89 +/- 0.23) > 5-HT (7.35 +/- 0.05) > sumatriptan (6.65 +/- 0.27). PAPP behaved as a partial agonist. 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin) was less potent, its maximal effect being not reached at 0.1 mM. Methiothepin. GR127935, (-)propranolol, rauwolscine and ketanserin were all devoid of intrinsic activity (up to 10 microM or 0.1 mM). Methiothepin (10 nM. 0.1 microM and 1 microM) antagonized 5-HT effect (pA2 8.57 +/- 0.44. Schild slope 1.17 +/- 0.21, n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Inhibition of noradrenaline release via presynaptic 5-HT1D alpha receptors in human atrium.

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.

5-Methoxytryptamine↗
PubMed1996

Effects of antimigraine drugs on retinal spreading depression.

It has been suggested that spreading depression may play a role in triggering classical migraine. In this study the retinal spreading depression was used as a pharmacological tool to test the neuronal effects of several common antimigraine drugs. As the chicken retina is void of any blood vessels the observed effects must be of pure neuronal origin. It is shown that propranolol, sumatriptan, methysergide, paracetamol and acetylsalicyclic acid decrease the propagation velocity of retinal spreading depression waves, accelerate the recovery of the optical and electrical signal and reduce the amplitude of the negative potential shift, concomitant with the spreading depression. Barbiturate increases the spreading velocity, and the amplitude of the potential shift. Ergotamine, clonidine, lisuride and iprazochrome have no significant influence on retinal spreading depression.

Acetaminophen↗
PubMed1995

Functional serotonin 5-HT1D receptors and 5-HT1D beta receptor mRNA expression in human umbilical vein endothelial cells.

Pharmacological evidence has suggested the presence of 5-hydroxytryptamine (5-HT, serotonin), 5-HT(1D) receptors on endothelial cells but these receptors have never been identified unambiguously on this type of cells. We now report that human umbilical vein endothelial cells (HUVEC) express 5-HT(1D) receptors coupled to inhibition of cyclic AMP formation. 5-HT and 5-HT(1D) receptor agonists 5-carboxamidotryptamine (5-CT) and sumatriptan were approximately equipotent at inhibiting forskolin-stimulated cyclic AMP accumulation in HUVEC (mean pEC50 7.6-8.2, maximal effect 30% inhibition). The 5-HT(1A) receptor antagonist, 8-OH-DPAT was clearly less potent (pEC50 6.2) and less efficacious. The selective 5-HT(1D) receptor agonist, GR127935 (1 nM) markedly inhibited the effect of 5-HT (apparent pK(B) 10.8). Reverse transcription-polymerase chain reaction analysis showed the mRNA for 5-HT(1D beta) receptors to be expressed in HUVEC. These results demonstrate the presence of functional 5-HT(1D) receptors and the expression of 5-HT(1D beta) receptor mRNA in HUVEC. They support the involvement of 5-HT(1D beta) receptors in endothelial-mediated responses to 5-HT.

8-Hydroxy-2-(di-n-propylamino)tetralin↗