bluuebunny/crossref_metadata_2025_split huggingface dataset:
High level of α2‐adrenoceptor in rat foetal liver and placenta is due to α2B‐subtype expression in haematopoietic cells of the erythrocyte lineage
Authors: Cussac Daniel , Schaak Stéphane , Denis Colette , Flordellis Christodoulos , Calise Denis , Paris Hervé 
Published: January 2005

Rat foetal liver contains large amounts of α2‐adrenoceptors. The present work aimed to identify the receptor subtype and the cell type accounting for high expression and to clarify the mechanisms responsible for the sharp decrease in hepatic receptivity occurring during the late stage of foetal development.
Binding experiments indicated that the density of α2‐adrenoceptors in the foetal liver (embryonic day 18; 615±155 fmol mg−1 of protein) is 18 fold higher than in newborn or adult (35.2±4.3 fmol mg−1). A high amount of receptor is also found in the placenta (443±53 fmol mg−1). In both tissues, the rank order of antagonists to inhibit radioligand binding matched the pharmacological profile of the α2B‐adrenoceptor and exclusively RNG transcripts were detected by RNase protection assays.
Isolation of cell fractions from foetal liver showed that α2B‐adrenoceptor is primarily expressed by haematopoietic cells. Consistent with this view, the receptor is found to be abundant in foetal blood, carried by reticulocytes. The expression in blood gradually declines to zero at 3 weeks of age and it is not recovered following induction of reticulocytosis in adults.
In foetal reticulocytes, a low proportion of the receptor population is coupled to G‐protein. The α2‐agonist UK14304 has a marginal effect on cyclic AMP level but significantly increases arachidonic acid release. The function of the receptor remains to be elucidated. However, together with observations on α2B‐knockout mice, the current finding strongly suggests a role for α2B‐adrenoceptor during foetal haematopoiesis in rodents.

British Journal of Pharmacology (2001) 133, 1387–1395; doi:10.1038/sj.bjp.0704203
Estimation of anti‐platelet drugs on human platelet aggregation with a novel whole blood aggregometer by a screen filtration pressure method
Authors: Sudo Toshiki , Ito Hideki , Ozeki Yasushi , Kimura Yukio 
Published: January 2005

The effects of anti‐platelet drugs on human whole blood aggregation were evaluated using a novel whole blood aggregometer by a screen filtration pressure (SFP) method.
The SFP whole blood aggregometer was found to successfully detect whole blood aggregation induced by ADP, collagen and TRAP by measuring the SFP of blood samples. The platelet aggregation threshold index (PATI), the concentration of agonist required with an inducing pressure rate of 50%, varied time‐dependently after collection of blood. High values for ADP and collagen were noted immediately after blood collection, suggesting low aggregation activity of platelets, and gradually increase thereafter.
Cilostazol (phosphodiesterase 3 inhibitor), dipyridamole, aspirin and tirofiban all inhibited whole blood aggregation in vitro. Inhibitory effects of cilostazol and dipyridamole, but not tirofiban, were markedly enhanced 6 or 7 fold by long pre‐incubation (60 min), compared with short pre‐incubation (2 min). Such enhancement was only observed with ADP‐ and not collagen‐induced whole blood aggregation. A similar phenomenon was also observed for aggregation with platelet rich plasma (PRP). Cilostazol inhibition of ADP‐induced platelet aggregation was more potent with PRP than whole blood (PATI200=3.80±0.95 μM for whole blood; 2.04±0.61 μM for PRP). Inhibitory effects of dipyridamole were attenuated in PRP without erythrocytes.
These results demonstrate that the SFP aggregometer can sensitively detect anti‐platelet aggregatory effects of various kinds of drugs. So that it is a useful tool for evaluation of anti‐platelet drugs.

British Journal of Pharmacology (2001) 133, 1396–1404; doi:10.1038/sj.bjp.0704204
Differential effects of chronic drug treatment on α3* and α7 nicotinic receptor binding sites, in hippocampal neurones and SH‐SY5Y cells
Authors: Ridley Diana L , Rogers Adrian , Wonnacott Susan 
Published: January 2005

The aim of this study was to compare the effects of chronic treatment (for 4 or 7 days) with nicotinic drugs and 20 mM KCl on numbers of surface α7 nicotinic AChR, identified by [125I]‐α bungarotoxin (α‐Bgt) binding, in primary hippocampal cultures and SH‐SY5Y cells. Numbers of α3* nicotinic AChR were also examined in SH‐SY5Y cells, using [3H]‐epibatidine, which is predicted to label the total cellular population of predominantly α3β2* nicotinic AChR under the conditions used.
All the nicotinic agonists examined, the antagonists d‐tubocurarine and methyllycaconitine, and KCl, upregulated [125I]‐α Bgt binding sites by 20–60% in hippocampal neurones and, where examined, SH‐SY5Y cells.
Upregulation of [125I]‐α‐Bgt binding sites by KCl was prevented by co‐incubation with the L‐type Ca2+ channel blocker verapamil or the Ca2+‐calmodulin dependent kinase II (CaM‐kinase II) inhibitor KN‐62. Upregulation of [125I]‐α‐Bgt binding sites by nicotine or 3,[(4‐dimethylamino) cinnamylidene] anabaseine maleate (DMAC) was insensitive to these agents.
[3H]‐Epibatidine binding sites in SH‐SY5Y cells were not affected by KCl but were upregulated in a verapamil‐insensitive manner by nicotine and DMAC. KN‐62 itself provoked a 2 fold increase in [3H]‐epibatidine binding. The inactive analogue KN‐04 had no effect, suggesting that CaM‐kinase II plays a role in regulating numbers of α3* nicotinic AChR.
These data indicate that numbers of α3* and α7 nicotinic AChR are modulated differently. Nicotinic agonists and KCl upregulate α7 nicotinic AChR through distinct cellular mechanisms, the latter involving L‐type Ca2+ channels and CaM‐kinase II. In contrast, α3* nicotinic AChR are not upregulated by KCl. This difference may reflect the distinct physiological roles proposed for α7 nicotinic AChR.

British Journal of Pharmacology (2001) 133, 1286–1295; doi:10.1038/sj.bjp.0704207
Proinflammatory characteristics of a nonpeptide bradykinin mimic, FR190997, in vivo
Authors: Hayashi Izumi , Ishihara Keiko , Kumagai Yuji , Majima Masataka 
Published: January 2005

Proinflammatory potency of the nonpeptide bradykinin (BK) B2 receptor agonist FR190997 (8‐[2,6‐dichloro‐3‐[N‐[(E)‐4‐(N‐methylcarbamoyl)cinnamidoacetyl]‐N‐methylamino]benzyloxy]‐2‐methyl‐4‐(2‐pyridylmethoxy)quinoline) was investigated.
Intradermal injection of FR190997 (0.03–3 nmol site−1) into dorsal skin of rats increased vascular permeability in a dose‐dependent manner. The effect was less than that of BK, but it was long‐acting and was inhibited by treatment with FR173657 (3 mg kg−1, p.o.). Captopril (10 mg kg−1, i.p.) did not enhance the plasma extravasation by FR190997 (0.3 nmol site−1) in the presence of soybean trypsin inhibitor (SBTI, 30 μg site−1).
Subcutaneous injection of FR190997 (3 nmol site−1) into the hindpaw of mice markedly induced paw swelling. The oedema lasted up to 3 h after the injection. Administration of indomethacin or NS‐398 (10 mg kg−1, i.p.) significantly reduced it at 3 h after the injection.
Simultaneous i.p. injection of prostaglandin (PG) E2 (1 nmol site−1) or beraprost sodium (0.5 nmol site−1) with FR190997 (5 nmol site−1) greatly enhanced frequency of writhing reactions in mice.
FR190997 (0.3–30 nmol kg−1, i.v.) showed less increase in airway opening pressure (Pao) in the guinea‐pig after i.v. injection. Furthermore, FR190997 (0.03–30 nmol) resulted in a very weak contraction of tracheal ring strips and lung parenchymal sections in vitro.
In mice sponge implants, topical application of FR190997 increased angiogenesis and granulation with enhanced expressions of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) mRNAs.
These results indicate that FR190997 has proinflammatory long‐lasting characteristics and it might be ‘a stable tool’ for studying the role of BK B2 receptor in vivo.

British Journal of Pharmacology (2001) 133, 1296–1306; doi:10.1038/sj.bjp.0704208
CGRP receptors mediating CGRP‐, adrenomedullin‐ and amylin‐induced relaxation in porcine coronary arteries. Characterization with ‘Compound 1’ (WO98/11128), a non‐peptide antagonist
Authors: Hasbak Philip , Sams Anette , Schifter Søren , Longmore Jenny , Edvinsson Lars 
Published: January 2005

Calcitonin gene‐related peptide (CGRP), amylin and adrenomedullin (AM) belong to the same family of peptides. Accumulating evidence indicate that the calcitonin (CT) receptor, the CT receptor‐like receptor (CRLR) and receptor‐activity‐modifying proteins (RAMPs) form the basis of all the receptors in this family of peptides.
Using reverse transcriptase–polymerase chain reaction the presence of mRNA sequences encoding the CRLR, RAMP1 and RAMP2 were demonstrated in porcine left anterior descending (LAD) coronary arteries, whereas porcine calcitonin (CT) receptor mRNA was not present. The partial porcine mRNA sequences shared 82–92% nucleotide identity with human sequences.
The human peptides αCGRP, βCGRP, AM and amylin induced relaxation with pEC50 values of 8.1, 8.1, 6.7 and 6.1 M respectively.
The antagonistic properties of a novel non‐peptide CGRP antagonist ‘Compound 1’ (WO98/11128), βCGRP8–37 and the proposed AM receptor antagonist AM22–52 were compared to the well‐known CGRP1 receptor antagonist αCGRP8–37.
The αCGRP8–37 and βCGRP8–37 induced concentration‐dependent (10−7–10−5 M) rightward shift of both the αCGRP and βCGRP concentration‐response curves. βCGRP8–37 (10−6 M) had the same effect as αCGRP8–37 (10−6 M), but with less potent rightward shift of the concentration‐response curves for αCGRP, AM and amylin.
Preincubation with ‘Compound 1’ (10−7–10−5 M) and AM22–52 (10−6 M) had no significant antagonistic effect.
In conclusion, the building blocks forming CGRP and AM receptors were present in the porcine LAD, whereas those of the amylin receptor were not. αCGRP, βCGRP, AM and amylin mediated vasorelaxation via the CGRP receptors. No functional response was detected to adrenomedullin via the adrenomedullin receptor.

British Journal of Pharmacology (2001) 133, 1405–1413; doi:10.1038/sj.bjp.0704210
In vivo evidence that protease‐activated receptors 1 and 2 modulate gastrointestinal transit in the mouse
Authors: Kawabata Atsufumi , Kuroda Ryotaro , Nagata Nanae , Kawao Naoyuki , Masuko Takashi , Nishikawa Hiroyuki , Kawai Kenzo 
Published: January 2005

Protease‐activated receptors (PARs) 1 and 2 modulate the gastric and intestinal smooth muscle motility in vitro. In the present study, we examined if activation of PAR‐2 and PAR‐1 could alter gastrointestinal transit in mice.
Intraperitoneal administration of the PAR‐2‐activating peptide SLIGRL‐NH2, but not the inactive control LSIGRL‐NH2, at 1–5 μmol kg−1, in combination with the aminopeptidase inhibitor amastatin at 2.5 μmol kg−1, facilitated gastrointestinal transit in a dose‐dependent manner. The human PAR‐1‐derived peptide SFLLR‐NH2 and the specific PAR‐1 agonist TFLLR‐NH2, but not the inactive control FSLLR‐NH2, at 2.5–10 μmol kg−1, in combination with amastatin, also promoted gastrointestinal transit.
The Ca2+‐activated, small conductance K+ channel inhibitor apamin at 0.01 μmol kg−1 significantly potentiated the actions of SLIGRL‐NH2 and TFLLR‐NH2 at subeffective doses.
The increased gastrointestinal transit exerted by either SLIGRL‐NH2 at 5 μmol kg−1 or TFLLR‐NH2 at 10 μmol kg−1 was completely abolished by the L‐type Ca2+ channel inhibitor verapamil at 61.6 μmol kg−1. In contrast, the tyrosine kinase inhibitor genistein at 18.5 μmol kg−1 failed to modify the effects of the agonists for PAR‐2 or PAR‐1.
These findings demonstrate that PAR‐1 and PAR‐2 modulate gastrointestinal transit in mice in vivo. Our data also suggest that the PAR‐1‐and PAR‐2‐mediated effects are modulated by apamin‐sensitive K+ channels and are dependent on activation of L‐type Ca2+ channels, but independent of tyrosine kinase. Our study thus provides novel evidence for the physiological and/or pathophysiological roles of PARs 1 and 2 in the digestive systems, most probably during inflammation.

British Journal of Pharmacology (2001) 133, 1213–1218; doi:10.1038/sj.bjp.0704211
Ca2+‐sensitizing effect is involved in the positive inotropic effect of troglitazone
Authors: Furuse Yoshiyuki , Ogino Kazuhide , Shimoyama Masaki , Sasaki Norihito , Hisatome Ichiro 
Published: January 2005

Troglitazone, an insulin sensitizing agent, has a direct positive inotropic effect. However, the mechanism of this effect remains unclear. Thus, we examined the inotropic effect of troglitazone while focusing on intracellular Ca2+ handling.
Troglitazone significantly increased peak isovolumic left ventricular pressure (LVPmax), peak rate of rise of LVP (dP/dtmax), peak rate of fall of LVP (dP/dtmin) in isolated rat hearts perfused at a constant coronary flow and heart rate. This inotropic effect of troglitazone was not inhibited by pretreatment with carbachol (muscarine receptor agonist), H89 (protein kinase A inhibitor), U73122 (phospholipase C inhibitor), H7 (protein kinase C inhibitor), verapamil (L‐type Ca2+ channel antagonist), thapsigargin (Ca2+‐adenosine triphosphatase inhibitor) or ryanodine (ryanodine receptor opener).
Radioimmunoassay showed that the cyclic adenosine monophosphate concentration in the left ventricle was not increased by troglitazone.
Whole‐cell patch clamp analysis revealed that troglitazone had no effect on inward Ca2+ currents in cardiomyocytes.
In fura‐2 loaded perfused rat hearts, troglitazone exerted its positive inotropic effect without increasing Ca2+ concentration.
These results suggest that neither the inward Ca2+ currents nor Ca2+ handling in the sarcoplasmic reticulum was involved in the inotropic effect of troglitazone. Furthermore, troglitazone exerted its positive inotropic effect without affecting the intracellular concentration of Ca2+.
In conclusion, the positive inotropic effect of troglitazone is mediated by a sensitization of Ca2+.

British Journal of Pharmacology (2001) 133, 1307–1313; doi:10.1038/sj.bjp.0704212
Effect of M40403 treatment of diabetic rats on endoneurial blood flow, motor nerve conduction velocity and vascular function of epineurial arterioles of the sciatic nerve
Authors: Coppey Lawrence J , Gellett Jill S , Davidson Eric P , Dunlap Joyce A , Lund Donald D , Salvemini Daniela , Yorek Mark A 
Published: January 2005

To further explore the effect of antioxidants in preventing diabetes‐induced vascular and neural dysfunction we treated streptozotocin‐induced diabetic rats daily with subcutaneous injections of 10 mg kg−1 of M40403 (n=11) and compared the results obtained from 17 control rats and 14 untreated diabetic rats. M40403 is a manganese(II) complex with a bis(cyclo‐hexylpyridine)‐substituted macrocyclic ligand that was designed to be a selective functional mimetic of superoxide dismutase. Thus, M40403 provides a useful tool to evaluate the roles of superoxide in disease states.
Treatment with M40403 significantly improved diabetes‐induced decrease in endoneurial blood flow, acetylcholine‐mediated vascular relaxation in arterioles that provide circulation to the region of the sciatic nerve, and motor nerve conduction velocity (P<0.05). M40403 treatment also reduced the appearance of superoxide in the aorta and epineurial vessels and peroxynitrite in epineurial vessels. Treating diabetic rats with M40403 reduced the diabetes‐induced increase in thiobarbituric acid reactive substances in serum but did not prevent the decrease in lens glutathione level. Treating diabetic rats with M40403 did not improve sciatic nerve Na+/K+ ATPase activity or the sorbitol, fructose or myo‐inositol content of the sciatic nerve.
These studies provide additional evidence that diabetes‐induced oxidative stress and the generation of superoxide and perhaps peroxynitrite may be partially responsible for the development of diabetic vascular and neural complications.

British Journal of Pharmacology (2001) 134, 21–29; doi:10.1038/sj.bjp.0704216
Pharmacological characterization of adenosine receptors in PGT‐β mouse pineal gland tumour cells
Authors: Suh Byung‐Chang , Kim Tae‐Don , Lee Jung‐Uek , Seong Je‐Kyung , Kim Kyong‐Tai 
Published: January 2005

The adenosine receptor in mouse pinealocytes was identified and characterized using pharmacological and physiological approaches.
Expression of the two adenosine receptor subtypes A2B and A3 was detected in mouse pineal glands and PGT‐β cells by polymerase chain reaction and nucleotide sequencing.
Adenosine and 5′‐N‐ethylcarboxamidoadenosine (NECA) evoked cyclic AMP generation but the A2A‐selective agonist 2‐(4‐(2‐carboxyethyl)phenylethylamino)adenosine‐5′‐N‐ethylcarboxamideadenosine (CGS 21680) and the A1‐specific agonists R‐N6‐(2‐phenylisopropyl)adenosine (R‐PIA) and N6‐cyclopentyladenosine (CPA) had little effect on intracellular cyclic AMP levels. The A2B receptor selective antagonists alloxazine and enprofylline completely blocked NECA‐mediated cyclic AMP accumulation.
Treatment of cells with the A3‐selective agonist N6‐(3‐iodobenzyl)‐5′‐(N‐methylcarbamoyl)adenosine (IB‐MECA) inhibited the elevation of the cyclic AMP level induced by NECA or isoproterenol in a concentration‐dependent manner with maximal inhibition of 40 – 50%. These responses were blocked by the specific A3 adenosine receptor antagonist MRS 1191. Pretreatment of the cells with pertussis toxin attenuated the IB‐MECA‐induced responses, suggesting that this effect occurred via the pertussis toxin‐sensitive inhibitory G proteins.
IB‐MECA also caused a concentration‐dependent elevation in [Ca2+]i and IP3 content. Both the responses induced by IB‐MECA were attenuated by treatment with U73122 or phorbol 12‐myristate 13‐acetate.
These data suggest the presence of both A2B and A3 adenosine receptors in mouse pineal tumour cells and that the A2B receptor is positively coupled to adenylyl cyclase whereas the A3 receptor is negatively coupled to adenylyl cyclase and also coupled to phospholipase C.

British Journal of Pharmacology (2001) 134, 132–142; doi:10.1038/sj.bjp.0704218
Differential effects of anandamide on acetylcholine release in the guinea‐pig ileum mediated via vanilloid and non‐CB1 cannabinoid receptors
Authors: Mang Christian F , Erbelding Doris , Kilbinger Heinz 
Published: January 2005

The effects of anandamide on [3H]‐acetylcholine release and muscle contraction were studied on the myenteric plexus‐longitudinal muscle preparation of the guinea‐pig ileum preincubated with [3H]‐choline.
Anandamide increased both basal [3H]‐acetylcholine release (pEC50 6.3) and muscle tone (pEC50 6.3). The concentration‐response curves for anandamide were shifted to the right by 1 μM capsazepine (pKB 7.5 and 7.6), and by the combined blockade of NK1 and NK3 tachykinin receptors with the antagonists CP99994 plus SR142801 (each 0.1 μM). The CB1 and CB2 receptor antagonists, SR141716A (1 μM) and SR144528 (30 nM), did not modify the facilitatory effects of anandamide.
Anandamide inhibited the electrically‐evoked release of [3H]‐acetylcholine (pEC50 5.8) and contractions (pEC50 5.2). The contractile response to the muscarinic agonist methacholine was not significantly affected by 10 μM anandamide.
The inhibitory effects of anandamide were not changed by either capsazepine (1 μM), SR144528 (30 nM) or CP99994 plus SR142801 (each 0.1 μM). SR141716A (1 μM) produced rightward shifts in the inhibitory concentration‐response curves for anandamide yielding pKB values of 6.6 and 6.2.
CP55940 inhibited the evoked [3H]‐acetylcholine release and contractions, and SR141716A (0.1 μM) shifted the concentration‐response curves of CP55940 to the right with pKB values of 8.4 and 8.9.
The experiments confirm the existence of release‐inhibitory CB1 receptors on cholinergic myenteric neurones. We conclude that anandamide inhibits the evoked acetylcholine release via stimulation of a receptor that is different from the CB1 and CB2 receptor. Furthermore, anandamide increases basal acetylcholine release via stimulation of vanilloid receptors located at primary afferent fibres.

British Journal of Pharmacology (2001) 134, 161–167; doi:10.1038/sj.bjp.0704220
Mechanism of action of angiotensin II in human isolated subcutaneous resistance arteries
Authors: Garcha Robinder S , Sever Peter S , Hughes Alun D 
Published: January 2005

Human isolated subcutaneous arteries were mounted in a myograph and isometric tension measured. In some experiments, intracellular calcium [Ca2+]i was also measured using fura‐2.
Angiotensin II (100 pM – 1 μM) increased [Ca2+]i and tone in a concentration‐dependent manner. The effects of angiotensin II (100 nM) were inhibited by an AT1‐receptor antagonist, candesartan (100 pM).
Ryanodine (10 μM), had no effect on angiotensin II‐induced responses, but removal of extracellular Ca2+ abolished angiotensin II‐induced rise in [Ca2+]i and tone. Inhibition of Ca2+ entry by Ni2+ (2 mM), also inhibited angiotensin II responses. The dihydropyridine, L‐type calcium channel antagonist, amlodipine (10 μM), only partially attenuated angiotensin II responses.
Inhibition of protein kinase C (PKC) by chelerythrine (1 μM), or by overnight exposure to a phorbol ester (PDBu; 500 nM) had no effect on angiotensin II‐induced contraction.
Genistein (10 μM), a tyrosine kinase inhibitor, inhibited angiotensin II‐induced contraction, but did not inhibit the rise in [Ca2+]i, suggesting that at this concentration it affected the calcium sensitivity of the contractile apparatus. Genistein did not affect responses to norepinephrine (NE) or high potassium (KPSS).
A selective MEK inhibitor, PD98059 (30 μM), inhibited both the angiotensin II‐induced contraction and rise in [Ca2+]i, but had no effect on responses to NE or KPSS.
AT1 activation causes Ca2+ influx via L‐type calcium channels and a dihydropyridine‐insensitive route, but does not release Ca2+ from intracellular sites. Activation of tyrosine kinase(s) and the ERK 1/2 pathway, but not classical or novel PKC, also play a role in angiotensin II‐induced contraction in human subcutaneous resistance arteries.

British Journal of Pharmacology (2001) 134, 188–196; doi:10.1038/sj.bjp.0704222
A possible role of lipoxygenase in the activation of vanilloid receptors by anandamide in the guinea‐pig bronchus
Authors: Craib Susan J , Ellington Heather C , Pertwee Roger G , Ross Ruth A 
Published: January 2005

In the absence of indomethacin, anandamide did not contract the guinea‐pig bronchus at concentrations up to 100 μM. In the presence of indomethacin (10 μM), anandamide induced concentration‐related contractions with a pEC50 value of 5.18±0.11. It was significantly less potent than capsaicin (pEC50 7.01±0.1). The anandamide uptake inhibitor AM404, produced only a 14.1±3.22% contraction at 100 μM. All experiments were conducted in the presence of PMSF (20 μM).
The vanilloid receptor antagonist, capsazepine (10 μM), significantly attenuated the contractile effect of anandamide, the response to 100 μM anandamide being 40.53±7.04% in the presence of vehicle and 1.57±8.93% in the presence of 10 μM capsazepine. The contractile actions of anandamide and AM404 were markedly enhanced by the peptidase inhibitor thiorphan.
The log concentration‐response curve of anandamide was unaltered by the CB1 receptor antagonist, SR141716A. The pEC50 values for anandamide were 4.88±0.08 and 5.17±0.19 in the presence of vehicle and SR141716A (1 μM) respectively.
The lipoxygenase inhibitors 5,8,11,14‐eicosatetraynoic acid (ETYA) and 5,8,11 eicosatriynoic acid (ETI) reduced the effect of 100 μM anandamide from 34.7±1.9% (vehicle) to 7.7±5% (ETYA, 10 μM) and from 41.85±4.25% (n=6) (vehicle) to 10.31±3.54 (n=6) (ETI, 20 μM). Neither inhibitor significantly affected contraction of the tissue by substance P.
This study provides evidence that anandamide acts on vanilloid receptors in the guinea‐pig isolated bronchus. These data raise the possibility that the contractile action of anandamide may be due, at least in part, to lipoxygenase metabolites of this fatty acid amide that are vanilloid receptor agonists.

British Journal of Pharmacology (2001) 134, 30–37; doi:10.1038/sj.bjp.0704223