bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mechanisms of AVP‐induced glucagon release in clonal α‐cells In‐R1‐G9: involvement of Ca2+‐dependent and ‐independent pathways
Authors: Yibchok‐anun Sirintorn , Cheng Henrique , Chen Ter‐Hsin , Hsu Walter H 
Published: January 2005

The mechanisms underlying AVP‐induced increase in [Ca2+]i and glucagon release in clonal α‐cells In‐R1‐G9 were investigated.
AVP increased [Ca2+]i and glucagon release in a concentration‐dependent manner. After the administration of AVP, glucagon was released within 30 s, quickly reached the maximum within 2 min, and maintained a steady‐state concentration for at least 15 min.
In Ca2+‐containing medium, AVP increased [Ca2+]i in a biphasic pattern; a peak followed by a sustained plateau. In Ca2+‐free medium, the Ca2+ response to AVP became monophasic with lower amplitude and no plateau. Both the basal and AVP‐induced glucagon releases were lower in the absence than in the presence of extracellular Ca2+. When [Ca2+]i was stringently deprived by BAPTA, a Ca2+ chelator, AVP still significantly increased glucagon release.
Pretreatment with thapsigargin, a microsomal Ca2+ ATPase inhibitor, abolished both the Ca2+ peak and sustained plateau.
AVP increased intracellular concentration of IP3.
U‐73122 (8 μM), a phospholipase C inhibitor, abolished AVP‐induced increases in [Ca2+]i, but only reduced AVP‐induced glucagon release by 39%.
Pretreatment with nimodipine, an L‐type Ca2+ channel blocker failed to alter AVP‐induced glucagon release or increase in [Ca2+]i.
The results suggest that AVP causes glucagon release through both Ca2+‐dependent and ‐independent pathways. For the Ca2+‐dependent pathway, the Gq protein activates phospholipase C, which catalyzes the formation of IP3. IP3 induces Ca2+ release from the endoplasmic reticulum, which, in turn, triggers Ca2+ influx. Both Ca2+ release and Ca2+ influx may contribute to AVP‐induced glucagon release.

British Journal of Pharmacology (2000) 129, 257–264; doi:10.1038/sj.bjp.0703037
Role of tachykinin NK2 receptors in normal and altered rectal sensitivity in rats
Authors: Toulouse M , Coelho A M , Fioramonti J , Lecci A , Maggi C , Buéno L 
Published: January 2005

Irritable bowel syndrome is characterized by visceral hyperalgesia commonly associated with stress and inflammatory processes. We investigated the role of tachykinin NK2 receptors in the ability of trinitrobenzenesulphonic acid (TNBS) and stress to enhance the sensitivity of the rat rectum to distension using a selective tachykinin NK2 receptor antagonist (MEN 11420).
Rats were fitted with electrodes implanted in the striated muscles of the abdomen. Rectal distension (RD) was performed with a balloon inflated by steps of 0.4 ml from 0 to 1.6 ml. Five groups were submitted to RD performed 3 days before and after intrarectal instillation of TNBS. Fifteen minutes before RD, rats were treated with saline or MEN 11420 (5–100 μg kg−1 i.v.). Two other groups, submitted to 2 h restraint or sham stress sessions were randomly treated i.v. with saline or MEN 11420 (10–200 μg kg−1) prior to RD applied 20 min later.
The basal response to RD was characterized by a significant increase in the number of abdominal contractions. This response occurred with a threshold volume of 0.8 ml and was dose‐dependently reduced by MEN 11420 (5–100 μg kg−1 i.v.). Rectal inflammation lowered the volume of distension producing abdominal contractions to 0.4 ml (allodynia). This effect was either reduced or suppressed by MEN 11420. A similar allodynia was observed after a stress session and this effect was reduced (49%) or suppressed by MEN 11420 at 200 and 100 μg kg−1, respectively.
Tachykinin NK2 receptors are involved in rectal hypersensitivity associated with inflammation and stress.

British Journal of Pharmacology (2000) 129, 193–199; doi:10.1038/sj.bjp.0703040
Tonic activation of A2A adenosine receptors unmasks, and of A1 receptors prevents, a facilitatory action of calcitonin gene‐related peptide in the rat hippocampus
Authors: Sebastião A M , Macedo M Paula , Ribeiro J A 
Published: January 2005

We investigated how manipulations of the degree of activation of adenosine A1 and A2A receptors influences the action of the neuropeptide, calcitonin gene‐related peptide (CGRP) on synaptic transmission in hippocampal slices. Field excitatory post‐synaptic potentials (EPSPs) from the CA1 area were recorded.
When applied alone, CGRP (1–30 nM) was without effect on field EPSPs. However, CGRP (10–30 nM) significantly increased the field EPSP slope when applied to hippocampal slices in the presence of the A1 receptor antagonist, 1,3‐dipropyl‐8‐cyclopenthyl xanthine (DPCPX, 10 nM), or in the presence of the A2A adenosine receptor agonist CGS 21680 (10 nM).
The A2A receptor antagonist, ZM 241385 (10 nM) as well as adenosine deaminase (ADA, 2 U ml−1), prevented the enhancement of field EPSP slope caused by CGRP (30 nM) in the presence of DPCPX (10 nM), suggesting that this effect of CGRP requires the concomitant activation of A2A adenosine receptors by endogenous adenosine.
The protein kinase‐A inhibitors, N‐(2‐guanidinoethyl)‐5‐isoquinolinesulfonamide (HA‐1004, 10 μM) and adenosine 3′,5′‐cyclic monophosphorothioate, Rp‐isomer (Rp‐cAMPS, 50 μM), as well as the inhibitor of ATP‐sensitive potassium (KATP) channels, glibenclamide (30 μM), prevented the facilitation of synaptic transmission caused by CGRP (30 nM) in the presence of DPCPX (10 nM), suggesting that this effect of CGRP involves both KATP channels and protein kinase‐A.
It is concluded that the ability of CGRP to facilitate synaptic transmission in the CA1 area of the hippocampus is under tight control by adenosine, with tonic A1 receptor activation by endogenous adenosine ‘braking’ the action of CGRP, and the A2A receptors triggering this action.

British Journal of Pharmacology (2000) 129, 374–380; doi:10.1038/sj.bjp.0703048
Differential effects of the tricyclic antidepressant amoxapine on glycine uptake mediated by the recombinant GLYT1 and GLYT2 glycine transporters
Authors: Núñez Enrique , López‐Corcuera Beatriz , Vázquez Jesús , Giménez Cecilio , Aragón Carmen 
Published: January 2005

We examined the effects of nine different tricyclic antidepressant drugs on the glycine uptake mediated by the glycine transporter 1b (GLYT1b) and glycine transporter 2a (GLYT2a) stably expressed in human embryonic kidney 293 cells. Desipramine, imipramine, clomipramine, nomifensine and mianserin had no effect on the activity of the glycine transporters. Doxepin, amitriptyline and nortriptyline inhibited the two transporter subtypes to a similar extent.
Amoxapine displayed a selective inhibition of GLYT2a behaving as a 10 fold more efficient inhibitor of this isoform than of GLYT1b.
Kinetic analysis of the initial rates of glycine uptake by GLYT2a as a function of either glycine, chloride or sodium concentration, in the absence and presence of amoxapine indicated that amoxapine behaved as a competitive inhibitor of both glycine and chloride and a mixed‐type inhibitor with respect to sodium.
A kinetic model was developed which explains adequately these data, and gives information about the order of binding of sodium and chloride ions to GLYT2a.
Our results may contribute to the development of the glycine transporter pharmacology. Additionally, the inhibition of the glycine uptake by GLYT2 is suggested to have some role in the sedative and psychomotor side effects of amoxapine.

British Journal of Pharmacology (2000) 129, 200–206; doi:10.1038/sj.bjp.0703049
Primary porcine enterocyte and hepatocyte cultures to study drug oxidation reactions
Authors: Bader A , Hansen T , Kirchner G , Allmeling C , Haverich A , Borlak J T 
Published: January 2005

Primary porcine hepatocytes and enterocytes were isolated and cultured in Williams' E medium for up to 10 days to investigate potential organ differences in the metabolism of the immunosuppressive compound tacrolimus (FK 506) and of two investigational drugs (KC11346 and KC12291). Using LC‐MS (FK506) and HPLC‐FL (KC 11346/12291) a number of metabolites with identical mass and/or identical retention time could be detected.
In the case of tacrolimus hepatocytes and enterocytes produced the same spectrum of metabolites, e.g. bisdemethyl‐tacrolimus, demethyl‐tacrolimus, demethyl‐hydroxy‐tacrolimus and hydroxy‐tacrolimus, albeit at varying intensities.
Treatment of enterocyte cultures with dexamethasone increased the overall metabolite formation very significantly (up to 36 fold).
The metabolism of tacrolimus was also studied with preparations of insect cells, that express specifically high levels of individual human cytochrome P450 (CYP) isoenzymes. All metabolites could be generated with microsomal preparations specifically expressing CYP3A4, but hydroxy‐tacrolimus was exclusively produced by CYP3A5.
In the case of the investigational drugs KC 11346 and KC 12291 only three metabolites were formed by cultured enterocytes whereas hepatocytes produced 10 and 20 metabolites, respectively.
When assessed at the protein level CYP1A and CYP3A were expressed in cultures of porcine enterocytes for up to 10 days but porcine hepatocytes expressed additionally CYP2C9/10.
In conclusion, primary enterocytes and hepatocytes can be successfully cultured for several days while maintaining mono‐oxygenase activity and may therefore be used as a tool for studying intestinal and hepatic metabolism.

British Journal of Pharmacology (2000) 129, 331–342; doi:10.1038/sj.bjp.0703062
A comparison of the anti‐inflammatory and anti‐nociceptive activity of nitroaspirin and aspirin
Authors: Al‐Swayeh O A , Clifford R H , Del Soldato P , Moore P K 
Published: January 2005

Nitroaspirin (2.5–50 mg kg−1, i.p. or 2.5–100 mg kg−1, p.o.) and aspirin (2.5–100 mg kg−1, i.p. or p.o.) exhibit anti‐inflammatory activity in the carrageenan‐induced hindpaw oedema model in the rat. When administered i.p., nitroaspirin was a more effective anti‐oedema agent than aspirin particularly in the ‘early’ phase (i.e. up to 60 min) of the response. The ED50 values for nitroaspirin and aspirin as inhibitors of the ‘late’ phase response (measured at 180 min) were 64.3 μmol kg−1 and >555 μmol kg−1, respectively. When administered p.o., neither nitroaspirin nor aspirin exhibited significant anti‐inflammatory activity in the ‘early’ phase and were of similar potency in the ‘late’ phase. Thus, at the highest dose used (100 mg kg−1, 360 min) orally administered nitroaspirin (aspirin in parenthesis) inhibited oedema formation by 46.9±1.6% (47.2±3.8%, both n=6, P<0.05).
Nitroaspirin and aspirin (25–200 mg kg−1, p.o.) caused dose‐related inhibition of the hyperalgesia to mechanical stimulation following intraplantar injection of carrageenan in the rat. ED50 values were 365 μmol kg−1 and 784 μmol kg−1, respectively. Neither drug influenced the threshold for mechanical stimulation in the contralateral (i.e. untreated) hindpaw.
Nitroaspirin and aspirin (2.5–100 mg kg−1, p.o.) caused dose‐related inhibition of acetic acid induced abdominal constrictions in the mouse (ED50 values of 154.7 μmol kg−1 and 242.8 μmol kg−1, respectively).
Nitroaspirin and aspirin (>200 mg kg−1, p.o.) reduced the ‘late’ phase (but not the ‘early’ phase) of the formalin‐induced hindpaw licking assay in the mouse. Similarly, nitroaspirin and aspirin (>50 mg kg−1, p.o.) prolonged tail withdrawal latency following application of a noxious heat stimulus in the mouse.

British Journal of Pharmacology (2000) 129, 343–350; doi:10.1038/sj.bjp.0703064
Differential regulation of mammalian brain‐specific proline transporter by calcium and calcium‐dependent protein kinases
Authors: Jayanthi Lankupalle D , Wilson Jennifer J , Montalvo Jocelyn , DeFelice Louis J 
Published: January 2005

This study examined the role of [Ca2+]I and Ca2+‐dependent kinases in the modulation of high‐affinity, mammalian brain‐specific L‐proline transporter (PROT).
β‐PMA (phorbol 12‐myristate 13‐acetate), an activator of protein kinase C (PKC), inhibits PRO uptake, and bisindolylmalemide I (BIM), a potent PKC inhibitor, prevents β‐PMA inhibition. Down‐regulation of PKC by chronic treatment with β‐PMA enhances PROT function indicating PROT regulation by tonic activity of PKC.
Thapsigargin, which increases [Ca2+]I levels by inhibiting Ca2+‐ATPase, inhibits PROT and exhibits additive inhibition when co‐treated with β‐PMA. KN‐62, a Ca2+/calmodulin‐dependent kinase II (CaMK II) inhibitor, but not BIM (a PKC inhibitor) prevents the inhibition by thapsigargin. These data suggest that PKC and CaMK II modulate PROT and that thapsigargin mediates its effect via CaMK II.
Thapsigargin raises [Ca2+]I and increases PRO‐induced current on a second time scale, whereas the inhibitory effect of thapsigargin occurs only after 10 min of treatment. These data suggest that Ca2+ differentially regulate PROT: Ca2+ initially enhances PRO transport but eventually inhibits transport function through CaMK II pathway.
Ca2+‐induced stimulation exemplifies the acute regulation of a neurotransmitter transporter, which may play a critical role in the profile of neurotransmitters during synaptic transmission

British Journal of Pharmacology (2000) 129, 465–470; doi:10.1038/sj.bjp.0703071
Characterization of MPP+ secretion across human intestinal Caco‐2 cell monolayers: role of P‐glycoprotein and a novel Na+‐dependent organic cation transport mechanism
Authors: Bleasby Kelly , Chauhan Seema , Brown Colin D A 
Published: January 2005

In the kidney, a number of transport proteins involved in the secretion of permanently charged organic cations have recently been cloned. To evaluate the possible similarities between intestine and kidney in the handling of organic cations we investigated the transport of 1‐methyl‐4‐phenylpyridinium (MPP+) across monolayers of intestinal Caco‐2 cells. MPP+ is a prototypic substrate of the cloned organic cation transporters hOCT1 and hOCT2.
In Caco‐2 cell monolayers, the basolateral to apical flux of MPP+ was significantly greater than the apical to basolateral flux, consistent with net secretion of MPP+.
Net secretion of MPP+ was abolished by addition of either 10 μM cyclosporin A or 100 μM verapamil to the apical membrane. In contrast, secretion of MPP+ was unaffected by addition of either TEA (2 mM) or decynium‐22 (2 μM) to either apical or basolateral membranes. These results suggest that MPP+ secretion is mediated primarily by P‐glycoprotein located at the apical membrane. We found no evidence of a role for hOCT1 or hOCT2 in the secretion of MPP+.
In addition to net secretion of MPP+, we found evidence of a Na+‐dependent MPP+ uptake mechanism at the apical membrane of Caco‐2 cells.
Na+‐dependent MPP+ uptake was sensitive to inhibition by the organic cations; decynium‐22 (2 μM), TEA (2 mM) and cimetidine (5 mM) but not by carnitine, guanidine or proline.
These results suggest that net secretion of MPP+ across the apical membrane of Caco‐2 cells is a function of the relative contributions of MPP+secretion mediated by P‐glycoprotein and MPP+ absorption mediated by a novel Na+‐dependent transport mechanism.

British Journal of Pharmacology (2000) 129, 619–625; doi:10.1038/sj.bjp.0703078
Prejunctional muscarinic inhibitory control of acetylcholine release in the human isolated detrusor: involvement of the M4 receptor subtype
Authors: D'Agostino Gianluigi , Bolognesi Maria L , Lucchelli Adele , Vicini Davide , Balestra Barbara , Spelta Valeria , Melchiorre Carlo , Tonini Marcello 
Published: January 2005

Experiments were carried out in human detrusor strips to characterize muscarinic receptor subtypes involved in the prejunctional regulation of acetylcholine (ACh) release from cholinergic nerve terminals, and in the postjunctional smooth muscle contractile response.
In detrusor strips preincubated with [3H]‐choline, electrical field stimulation (600 pulses) delivered in six trains at 10 Hz produced a tritium outflow and a contractile response. In the presence of 10 μM paraoxon (to prevent ACh degradation) the tritium outflow was characterized by HPLC analysis as [3H]‐ACh (76%) and [3H]‐choline (24%).
Electrically‐evoked [3H]‐ACh release was abolished by tetrodotoxin (TTX: 300 nM) and unaffected by hexamethonium (10 μM), indicating a postganglionic event. It was reduced by physostigmine (100 nM) and the muscarinic receptor agonist, muscarone (10 nM–1 μM), and enhanced by atropine (0.1–100 nM). These findings indicate the presence of a muscarinic negative feedback mechanism controlling ACh release.
The effects of various subtype‐preferring muscarinic receptor antagonists were evaluated on [3H]‐ACh release and muscle contraction. The rank potency (−log EC50) orders at pre‐ and postjunctional level were: atropine 4‐diphenyl‐acetoxy‐N‐piperidine (4‐DAMP)>mamba toxin 3 (MT‐3)>tripitramine>para‐fluorohexahydrosiladiphenidol (pF‐HHSiD)methoctraminepirenzepine>tripinamide, and atropine4‐DAMP>pF‐HHSiD>>pirenzepine=tripitramine>tripinamide>methoctramine>>MT‐3, respectively.
The comparison of pre‐ and post‐junctional potencies and the relationship analysis with the affinity constants at human cloned muscarinic receptor subtypes indicates that the muscarinic autoreceptor inhibiting ACh release in human detrusor is an M4 receptor, while the receptor involved in muscular contraction belongs to the M3 subtype.

British Journal of Pharmacology (2000) 129, 493–500; doi:10.1038/sj.bjp.0703080
Differential tetraethylammonium sensitivity of KCNQ1–4 potassium channels
Authors: Hadley J K , Noda M , Selyanko A A , Wood I C , Abogadie F C , Brown D A 
Published: January 2005

In Shaker‐group potassium channels the presence of a tyrosine residue, just downstream of the pore signature sequence GYG, determines sensitivity to tetraethylammonium (TEA). The KCNQ family of channels has a variety of amino acid residues in the equivalent position. We studied the effect of TEA on currents generated by KCNQ homomers and heteromers expressed in CHO cells. We used wild‐type KCNQ1–4 channels and heteromeric KCNQ2/3 channels incorporating either wild‐type KCNQ3 subunits or a mutated KCNQ3 in which tyrosine replaced threonine at position 323 (mutant T323Y). IC50 values were (mM): KCNQ1, 5.0; KCNQ2, 0.3; KCNQ3, >30; KCNQ4, 3.0; KCNQ2+KCNQ3, 3.8; and KCNQ2+KCNQ3(T323Y), 0.5. While the high TEA sensitivity of KCNQ2 may be conferred by a tyrosine residue lacking in the other channels, the intermediate TEA sensitivity of KCNQ1 and KCNQ4 implies that other residues are also important in determining TEA block of the KCNQ channels.British Journal of Pharmacology (2000) 129, 413–415; doi:10.1038/sj.bjp.0703086
Comparison of novel cannabinoid partial agonists and SR141716A in the guinea‐pig small intestine
Authors: Coutts Angela A , Brewster Nicola , Ingram Tracey , Razdan Raj K , Pertwee Roger G 
Published: January 2005

The controversial nature of the CB1 receptor antagonist, SR141716A, in the guinea‐pig small intestine was investigated by comparing it with four analogues of Δ8‐tetrahydrocannabinol (Δ8‐THC): O‐1184, O‐1238, O‐584 and O‐1315.
These compounds (10–1000 nM) inhibited the electrically‐evoked contractions with a rank order of potency of O‐1238>O‐1184>O‐584>O‐1315. Log concentration‐response curves for O‐1238, O‐1184 and O‐1315 were significantly shifted to the right by SR141716A and the maxima were significantly less than that of the CB1 agonist, WIN55212‐2, an indication of partial agonism.
Partial saturation of the triple bond in O‐1184 to a cis double bond (O‐1238) increased its potency as an agonist (pEC50 from 6.42 to 7.63) and as an antagonist of WIN55212‐2, (pKB, from 8.36 to 9.49). Substitution of the terminal azide group by an ethyl group (O‐584) or removal of the phenolic hydroxyl group (O‐1315) had no significant effect on the agonist or antagonist potency. None of these analogues increased the twitch response in a manner resembling that of SR141716A.
O‐1184 (10 and 100 nM) shifted the log concentration‐response curve of WIN55212‐2 for inhibition of the twitch responses to the right with pKB values of 8.29 and 8.38, respectively.
We conclude that these Δ8‐THC analogues behave as partial agonists rather than silent antagonists at CB1 binding sites in this tissue. There was no evidence of antagonism of endocannabinoids thus supporting the hypothesis that, in this tissue, SR141716A is an inverse agonist of constitutively active CB1 receptors.

British Journal of Pharmacology (2000) 129, 645–652; doi:10.1038/sj.bjp.0703094
M‐type K+ currents in rat cultured thoracolumbar sympathetic neurones and their role in uracil nucleotide‐evoked noradrenaline release
Authors: Nörenberg W , Von Kügelgen I , Meyer A , Illes P , Starke K 
Published: January 2005

Cultured sympathetic neurones are depolarized and release noradrenaline in response to extracellular ATP, UDP and UTP. We examined the possibility that, in neurones cultured from rat thoracolumbar sympathetic ganglia, inhibition of the M‐type potassium current might underlie the effects of UDP and UTP.
Reverse transcriptase‐polymerase chain reaction indicated that the cultured cells contained mRNA for P2Y2‐, P2Y4‐ and P2Y6‐receptors as well as for the KCNQ2‐ and KCNQ3‐subunits which have been suggested to assemble into M‐channels.
In cultures of neurones taken from newborn as well as from 10 day‐old rats, oxotremorine, the M‐channel blocker Ba2+ and UDP all released previously stored [3H]‐noradrenaline.
The neurones possessed M‐currents, the kinetic properties of which were similar in neurones from newborn and 9–12 day‐old rats.
UDP, UTP and ATP had no effect on M‐currents in neurones prepared from newborn rats. Oxotremorine and Ba2+ substantially inhibited the current.
ATP also had no effect on the M‐current in neurones prepared from 9–12 day‐old rats. Oxotremorine and Ba2+ again caused marked inhibition. In contrast to cultures from newborn animals, UDP and UTP attenuated the M‐current in neurones from 9–12 day‐old rats; however, the maximal inhibition was less than 30%.
The results indicate that inhibition of the M‐current is not involved in uracil nucleotide‐induced transmitter release from rat cultured sympathetic neurones during early development. M‐current inhibition may contribute to release at later stages, but only to a minor extent. The mechanism leading to noradrenaline release by UDP and UTP remains unknown.

British Journal of Pharmacology (2000) 129, 709–723; doi:10.1038/sj.bjp.0703096
Effects of local delivery of trapidil on neointima formation in a rabbit angioplasty model
Authors: Zacharowski Kai , Schneidmüller Dorien , Ibe Waltraut , Großer Tilo , Buerke Michael , Meyer Jürgen , Darius Harald 
Published: January 2005

Smooth muscle cell (SMC) proliferation can result in luminal reduction of a vessel following balloon angioplasty. This study was designed (i) to determine if local administration of trapidil (triazolopyrimidine) into a vessel wall reduces neointima formation, and (ii) to explore the mechanism involved in the subsequent reduction in cell proliferation.
Following balloon angioplasty in 40 anaesthetized New Zealand White rabbits, trapidil (50–200 mg) or its vehicle (saline) was injected into the dilated vessel wall of the right femoral artery. Experimental groups and time of investigation: (I) vehicle (2 weeks, n=3), (II) trapidil‐100 mg (2 weeks, n=3), (III) vehicle (3 weeks, n=8), (IV) trapidil‐50 mg (3 weeks, n=5); (V) trapidil‐100 mg (3 weeks, n=9) or (V) trapidil‐200 mg (3 weeks, n=7).
After 2 weeks, there was a significant reduction of intimal hyperplasia (expressed as intima to media area ratio) in the trapidil group compared with vehicle (0.44±0.04 vs 0.93±0.04, *P<0.05) and also a significant reduction in cell proliferation (% ratio of BrdU‐positive cells to total cell number: vehicle 14±2% vs trapidil 6±1%, *P<0.05).
After 3 weeks, there was a dose‐dependent reduction of intimal hyperplasia in the trapidil groups compared with vehicle (trapidil 50 mg 1.14±0.04; trapidil 100 mg 0.91±0.09*; trapidil 200 mg 0.77±0.09* vs vehicle 1.67±0.23, *P<0.05).
Thus, the local administration of trapidil to the rabbit femoral artery reduces the neointima formation, which occurs 2 or 3 weeks after balloon angioplasty via a mechanism, which is dependent on inhibition of cell proliferation.

British Journal of Pharmacology (2000) 129, 566–572; doi:10.1038/sj.bjp.0703098