bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphological and functional in vitro and in vivo characterization of the mouse corpus cavernosum
Authors: Mizusawa Hiroya , Hedlund Petter , Håkansson Anders , Alm Per , Andersson Karl‐Erik 
Published: January 2005

In normal mice, the distribution of adrenergic, cholinergic, some peptidergic, and neuronal nitric oxide synthase (nNOS)‐containing nerves were investigated. Functional in vitro correlates were obtained. An in vivo model was developed in which erectile haemodynamics in response to drugs or nerve‐stimulation were studied.
Immunoreactivities for vesicular acetylcholine transporter protein (VAChT), nNOS‐, and vasoactive intestinal polypeptide (VIP), co‐existed in nerve fibres and terminal varicosities. Immunoreactivities for neuropeptide Y (NPY) and tyrosine hydroxylase (TH) were found in the same nerve structures.
Chemical sympathectomy abolished TH‐ and NPY‐IR nerve structures in cavernous smooth muscle bundles. The distribution of calcitonin gene‐related peptide (CGRP)‐, nNOS‐, VAChT‐ and VIP‐IR nerve structures was unchanged.
In endothelial cells of the central and helicine arteries, veins and venules, intense immunoreactivity for endothelial NOS (eNOS) was observed. No distinct eNOS‐IR cells were found lining the cavernous sinusoids.
In vitro, nerve‐induced relaxations were verified, and endothelial NO/cyclic GMP‐mediated relaxant responses were established. VIP and CGRP had small relaxant effects. A functioning adenylate cyclase/cyclic AMP pathway was confirmed.
Neuronal excitatory responses were abolished by prazosin, or forskolin. VIP and CGRP counteracted contractions, whereas NPY and scopolamine enhanced excitatory responses.
In vivo, erectile responses were significantly attenuated by L‐NAME (50 mg kg−1) and facilitated by sildenafil (200 μg kg−1).
It is concluded that the mouse is a suitable model for studies of erectile mechanisms in vitro and in vivo.

British Journal of Pharmacology (2001) 132, 1333–1341; doi:10.1038/sj.bjp.0703938
[125I]‐(Pyr1)Apelin‐13 is a novel radioligand for localizing the APJ orphan receptor in human and rat tissues with evidence for a vasoconstrictor role in man
Authors: Katugampola Sidath D , Maguire Janet J , Matthewson Stewart R , Davenport Anthony P 
Published: January 2005

We have determined the binding characteristics of [125I]‐(Pyr1)Apelin‐13, a putative ligand for the APJ orphan receptor in human cardiovascular and rat tissue and investigated the functional properties of (Pyr1)Apelin‐13 in human saphenous vein.
The binding of [125I]‐(Pyr1)Apelin‐13 to sections of human heart tissue was time dependent and rapid at 23°C. Data were fitted to a single site model with an association rate constant (kobs) of 0.115 min−1. [125I]‐(Pyr1)Apelin‐13 also dissociated from a single site with a dissociation rate constant of 0.0105 min−1.
In saturation binding experiments [125I]‐(Pyr1)Apelin‐13 bound to human left ventricle with a KD value of 0.35±0.08 nM, Bmax of 4.3±0.9 fmol mg−1 protein with a Hill slope of 0.97±0.04 and to the right atria with a KD of 0.33±0.09 nM, Bmax of 3.1±0.6 fmol mg−1 protein and a Hill slope of 0.93±0.05.
[125I]‐(Pyr1)Apelin‐13 binding sites were localized using autoradiography to human cardiovascular tissue, including coronary artery, aorta and saphenous vein grafts. In rat tissue a high density of receptors were localized to the molecular layer of the rat cerebellum, rat lung, rat heart and low levels in the rat kidney cortex.
(Pyr1)Apelin‐13 potently contracted human saphenous vein with a pD2 value of 8.4±0.2 (n=8). The maximum response elicited by the peptide was 22.6±6% of 100 mM KCl.
We provide the first evidence of APJ receptor expression, relative densities and functional properties of (Pyr1)Apelin‐13 in human cardiovascular tissue.

British Journal of Pharmacology (2001) 132, 1255–1260; doi:10.1038/sj.bjp.0703939
Vascular endothelial growth factor and the in vivo increase in plasma extravasation in the hamster cheek pouch
Authors: Félétou Michel , Staczek Joanna , Duhault Jacques 
Published: January 2005

The purpose of this study in the hamster cheek pouch was to determine whether or not vascular endothelial growth factor (VEGF) induced changes in plasma extravasation and if so, the mechanism(s) involved.
The cheek pouch microcirculatory bed of the anaesthetized hamster was directly observed under microscope and the number of vascular leakage sites, as shown by fluorescein isothiocyanate (FITC‐dextran, 150 kD) extravasation, was counted. Drugs and VEGF were applied topically. VEGF from 0.05 to 0.5 μg ml−1 (1.2 to 12 nM) produced a dose‐dependent increase in the number of microvascular leakage sites from virtually none in basal conditions to up to 250 in some pouches. The effects of VEGF (0.1 μg ml−1 or 2.4 nM) were blocked in a concentration‐dependent manner by the non‐specific heparin growth factor antagonist TBC‐1635 (0.1, 1 and 3μM). The placenta growth factor (PlGF‐1: 0.1 and 0.5 μg ml−1 or 3.4 and 17 nM) did not increase plasma extravasation, per se, but abolished the effects of VEGF (2.4 nM).
The increases in microvascular leakage produced by VEGF (2.4 nM) were partially but significantly (P<0.05) inhibited by genistein (5 and 10 μM, up to 33% inhibition), LY 294002 (30 μM, 41%), bisindolylmaleimide (1 μM, 65%) and virtually abolished by indomethacin (3 μM, 88%) and L‐nitro‐arginine (10 μM, 95%), these drugs being inhibitors of tyrosine kinase, phosphatidylinositol‐3‐kinase, protein kinase C, cyclo‐oxygenase and nitric oxide synthase respectively. None of these inhibitors, at the concentration tested, induced alone an increase in plasma extravasation.
These results indicate that the VEGF‐induced plasma extravasation may involve the stimulation of VEGF‐R2 (Flk‐1/KDR) and the activation of phosphatidylinositol‐3‐kinase and protein kinase C. The production of both nitric oxide and prostaglandin is required to observe an increase in vascular leakage.

British Journal of Pharmacology (2001) 132, 1342–1348; doi:10.1038/sj.bjp.0703941
Role of nitric oxide synthases in the infarct size‐reducing effect conferred by heat stress in isolated rat hearts
Authors: Arnaud Claire , Laubriet Aline , Joyeux Marie , Godin‐Ribuot Diane , Rochette Luc , Demenge Pierre , Ribuot Christophe 
Published: January 2005

Nitric oxide (NO) donors are known to induce both delayed cardioprotection and myocardial heat stress protein (HSP) expression. Moreover, heat stress (HS), which also protects myocardium against ischaemic damages, is associated with a NO release. Therefore, we have investigated the implication of NO in HS‐induced resistance to myocardial infarction, in the isolated rat heart model.
Rats were divided in six groups (n=10 in each group), subjected or not to heat stress (42°C internal temperature, 15 min) and treated or not with nitro‐L‐arginine‐methylester (L‐NAME) a non‐selective inhibitor of NO synthase isoforms, or L‐N6‐(1‐imino‐ethyl)lysine (L‐NIL), a selective inhibitor of the inducible NO synthase. Twenty‐four hours after heat stress, their hearts were isolated, retrogradely perfused, and subjected to a 30‐min occlusion of the left coronary artery followed by 120 min of reperfusion.
Infarct‐to‐risk ratio was significantly reduced in HS (18.7±1.6%) compared to Sham (33.0±1.7%) hearts. This effect was abolished in L‐NAME‐treated (41.7±3.1% in HS+L‐NAME vs 35.2±3.0% in Sham+L‐NAME) and L‐NIL‐treated (36.1±3.4% in HS+L‐NIL vs 42.1±4.6% in Sham+L‐NIL) groups. Immunohistochemical analysis of myocardial HSP 27 and 72 showed an HS‐induced increase of these proteins, which was not modified by L‐NAME pretreatment.
We conclude that NO synthases, and in particular the inducible isoform, appear to play a role in the heat stress‐induced cardioprotection, independently of HSP 27 and 72 levels. Further investigations are required to elucidate the precise role of HSPs in this adaptive response.

British Journal of Pharmacology (2001) 132, 1845–1851; doi:10.1038/sj.bjp.0703942
Inducible nitric oxide synthase (iNOS) activity promotes ischaemic skin flap survival
Authors: Kane Anthony J , Barker Jane E , Mitchell Geraldine M , Theile David R B , Romero Rosalind , Messina Aurora , Wagh Milind , Fraulin Frankie O G , Morrison Wayne A , Stewart Alastair G 
Published: January 2005

We have examined the role of nitric oxide (NO) in a model of functional angiogenesis in which survival of a skin flap depends entirely on angiogenesis to provide an arterial blood supply to maintain tissue viability.
The different effects of nitric oxide synthase (NOS) inhibitors on rat skin flap survival appeared to be explained on the basis of their NOS isoform selectivity. Skin flap survival was decreased by iNOS‐selective (inducible NOS) inhibitors, S‐methyl‐isothiourea, aminoguanidine and aminoethylthiorea; unaffected by the non‐selective inhibitor nitro‐imino‐L‐ornithine; and enhanced by the cNOS (constitutive NOS, that is endothelial NOS (eNOS) and neuronal NOS (nNOS)) inhibitor, nitro‐L‐arginine methyl ester.
Skin flap survival was reduced in mice with targeted disruption of the iNOS gene (iNOS knockout mice), and the administration of nitro‐L‐arginine methyl ester significantly increased flap survival in iNOS knockout mice (P<0.05).
iNOS immunoreactivity was identified in mast cells in the angiogenic region. Immunoreactive vascular endothelial growth factor (VEGF) and basic fibroblast growth factor were also localized to mast cells.
The combination of interferon‐γ and tumour necrosis factor‐α induced NO production and increased VEGF levels in mast cells cultured from bone marrow of wild‐type, but not iNOS KO mice.
The increased tissue survival associated with the capacity for iNOS expression may be related to iNOS‐dependent enhancement of VEGF levels and an ensuing angiogenic response. Our results provide both pharmacological and genetic evidence that iNOS activity promotes survival of ischaemic tissue.

British Journal of Pharmacology (2001) 132, 1631–1638; doi:10.1038/sj.bjp.0703944
Evidence for functionally active protease‐activated receptor‐4 (PAR‐4) in human vascular smooth muscle cells
Authors: Bretschneider E , Kaufmann R , Braun M , Nowak G , Glusa E , Schrör K 
Published: January 2005

This study investigates, whether in addition to the protease‐activated receptor‐1 (PAR‐1), PAR‐4 is present in vascular smooth muscle cells (SMC) of the human saphenous vein and whether this receptor is functionally active. PAR‐1 and PAR‐4 are stimulated by thrombin and by the synthetic peptides SFLLRN and GYPGQV, respectively.
mRNAs for both, PAR‐1 and PAR‐4, were detected in the SMC by using reverse transcriptase polymerase chain reaction (RT – PCR).
Treatment of the SMC with GYPGQV (200 μM) resulted in a transient increase in free intracellular calcium. This calcium signal was completely abolished after a preceding challenge with thrombin (10 nM), indicating homologous receptor desensitization.
Stimulation of the SMC with 10 nM thrombin or 200 μM SFLLRN caused a time‐dependent activation of the extracellular signal‐regulated kinases‐1/2 (ERK‐1/2) with a maximum at 5 min. In contrast, 100 nM thrombin as well as 200 μM of GYPGQV induced a prolonged phosphorylation of ERK‐1/2 with a maximum at 60 min. These data suggest that PAR‐1 and PAR‐4 are activated by thrombin at distinct concentrations and with distinct kinetics.
GYPGQV stimulated [3H]‐thymidine incorporation in SMC. At 500 μM, the peptide increased DNA synthesis 2.5 fold above controls. A comparable mitogenic effect was obtained after stimulation of the SMC by 10 nM thrombin or 100 μM SFLLRN, respectively.
These data indicate that a functionally active PAR‐4 is present in SMC and, in addition to PAR‐1, might contribute to thrombin‐induced mitogenesis.

British Journal of Pharmacology (2001) 132, 1441–1446; doi:10.1038/sj.bjp.0703947
A nitric oxide‐dopamine link pathway in organum vasculosum laminae terminalis of rat brain exerts control over blood pressure
Authors: Chang C‐P , Pan S‐P , Lin M‐T 
Published: January 2005

Experiments were carried out to explore the possible role played by the nitric oxide (NO) and dopamine (DA) system in the organum vasculosum laminae terminalis (OVLT) of rat brain in arterial pressure regulation.
Intracerebroventricular (ICV) administration of NO donors such as hydroxylamine or sodium nitro‐prusside (SNP) caused an up to 59 mmHg decrease in blood pressure (BP) and a decrease in DA release (measured by nafion coated carbon fibre electrodes in combination with voltammetry) in the OVLT. In contrast, ICV administration of NG‐nitro‐L‐arginine methyl ester (L‐NAME; a constitutive NO synthase inhibitor) or 7‐nitroindazol (a neuronal NO synthase inhibitor) caused an up to 98 mmHg increase in BP and an increase in DA release in the OVLT.
Intra‐OVLT injection of amphetamine (0.1 – 0.3 mg), SKF 38393 (a DA D1 receptor agonist; 0.01 – 0.03 mg), or apomorphine (a DA D2,3 receptor agonist; 0.01 – 0.03 mg) caused an increase in BP. On the other hand, intra‐OVLT injection of SCH23390 (a DA D1 receptor antagonist; 0.005 – 0.020 mg) or haloperidol (0.005 – 0.020 mg) caused a decrease in BP.
The pressor effects induced by intra‐OVLT administration of L‐NAME were attenuated by pretreatment with intra‐OVLT injection of haloperidol, SCF23390, or 6‐hydroxydopamine. In the contrast, the hydroxylamine‐, 8‐Br‐cGMP‐ or SNP‐induced depressor effects were attenuated by pretreatment with intra‐OVLT injection of amphetamine, SKF 38393 or apomorphine.
The data suggest that activation of a NO‐DA link pathway within the OVLT of rat brain exerts control over blood pressure.

British Journal of Pharmacology (2001) 132, 1524–1530; doi:10.1038/sj.bjp.0703948
Glucocorticoids inhibit lipopolysaccharide‐induced up‐regulation of arginase in rat alveolar macrophages
Authors: Klasen Stefanie , Hammermann Rainer , Fuhrmann Margarita , Lindemann Dirk , Beck Karl‐Friedrich , Pfeilschifter Josef , Racké Kurt 
Published: January 2005

As arginase by limiting nitric oxide (NO) synthesis may play a role in airway hyperresponsiveness and glucocorticoids are known to induce the expression of arginase I in hepatic cells, glucocorticoid effects on arginase in alveolar macrophages (AMΦ) were studied.
Rat AMΦ were cultured in absence or presence of test substances. Thereafter, nitrite accumulation, arginase activity, and the expression pattern of inducible NO synthase, arginase I and II mRNA (RT – PCR) and proteins (immunoblotting) were determined.
Lipopolyssacharides (LPS, 20 h) caused an about 2 fold increase in arginase activity, whereas interferon‐γ (IFN‐γ), like LPS a strong inducer of NO synthesis, had no effect.
Dexamethasone decreased arginase activity by about 25% and prevented the LPS‐induced increase. Mifepristone (RU‐486) as partial glucocorticoid receptor agonist inhibited LPS‐induced increase by 45% and antagonized the inhibitory effect of dexamethasone.
Two different inhibitors of the NF‐κB‐pathway also prevented LPS‐induced increase in arginase activity.
Rat AMΦ expressed mRNA and protein of arginase I and II, but arginase I expression was stronger. Arginase I mRNA and protein was not affected by IFN‐γ, but increased by LPS and this effect was prevented by dexamethasone. Both, LPS and IFN‐γ enhanced the levels of arginase II mRNA and protein, effects also inhibited by dexamethasone. As IFN‐γ did not affect total arginase activity, arginase II may represent only a minor fraction of total arginase activity.
In rat AMΦ glucocorticoids inhibit LPS‐induced up‐regulation of arginase activity, an effect which may contribute to the beneficial effects of glucocorticoids in the treatment of inflammatory airway diseases.

British Journal of Pharmacology (2001) 132, 1349–1357; doi:10.1038/sj.bjp.0703951
SB‐334867‐A: the first selective orexin‐1 receptor antagonist
Authors: Smart D , Sabido‐David C , Brough S J , Jewitt F , Johns A , Porter R A , Jerman J C 
Published: January 2005

The pharmacology of various peptide and non‐peptide ligands was studied in Chinese hamster ovary (CHO) cells stably expressing human orexin‐1 (OX1) or orexin‐2 (OX2) receptors by measuring intracellular calcium ([Ca2+]i) using Fluo‐3AM. Orexin‐A and orexin‐B increased [Ca2+]i in CHO‐OX1 (pEC50=8.38±0.04 and 7.26±0.05 respectively, n=12) and CHO‐OX2 (pEC50=8.20±0.03 and 8.26±0.04 respectively, n=8) cells. However, neuropeptide Y and secretin (10 pM – 10 μM) displayed neither agonist nor antagonist properties in either cell‐line. SB‐334867‐A (1‐(2‐Methyylbenzoxanzol‐6‐yl)‐3‐[1,5]naphthyridin‐4‐yl‐urea hydrochloride) inhibited the orexin‐A (10 nM) and orexin‐B (100 nM)‐induced calcium responses (pKB=7.27±0.04 and 7.23±0.03 respectively, n=8), but had no effect on the UTP (3 μM)‐induced calcium response in CHO‐OX1 cells. SB‐334867‐A (10 μM) also inhibited OX2 mediated calcium responses (32.7±1.9% versus orexin‐A). SB‐334867‐A was devoid of agonist properties in either cell‐line. In conclusion, SB‐334867‐A is a non‐peptide OX1 selective receptor antagonist.British Journal of Pharmacology (2001) 132, 1179–1182; doi:10.1038/sj.bjp.0703953
Differential modulation of endothelin ligand‐induced contraction in isolated tracheae from endothelin B (ETB) receptor knockout mice
Authors: Hay Douglas W P , Douglas Stephen A , Ao Zhaohui , Moesker Rodney M , Self Glenn J , Rigby Paul J , Luttmann Mark A , Goldie Roy G 
Published: January 2005

The role of endothelin B (ETB) receptors in mediating ET ligand‐induced contractions in mouse trachea was examined in ETB receptor knockout animals.
Autoradiographic binding studies, using [125I]‐ET‐1, confirmed the presence of ETA receptors in tracheal and bronchial airway smooth muscle from wild‐type (+/+) and homozygous recessive (−/−) ETB receptor knockout mice. In contrast, ETB receptors were not detected in airway tissues from (−/−) mice.
In tracheae from (+/+) mice, the rank order of potencies of the ET ligands was sarafotoxin (Stx) S6c>ET‐1>ET‐3; Stx S6c had a lower efficacy than ET‐1 or ET‐3. In tissues from (−/−) mice there was no response to Stx S6c (up to 0.1 μM), whereas the maximum responses and potencies of ET‐1 and ET‐3 were similar to those in (+/+) tracheae. ET‐3 concentration‐response curve was biphasic in (+/+) tissues (via ETA and ETB receptor activation), and monophasic in (−/−) preparations (via stimulation of only ETA receptors).
In (+/+) preparations SB 234551 (1 nM), an ETA receptor‐selective antagonist, inhibited the secondary phase, but not the first phase, of the ET‐3 concentration‐response curve, whereas A192621 (100 nM), an ETB receptor‐selective antagonist, had the opposite effect. In (−/−) tissues SB 234551 (1 nM), but not A192621 (100 nM), produced a rightward shift in ET‐3 concentration‐response curves.
The results confirm the significant influence of both ETA and ETB receptors in mediating ET‐1‐induced contractions in mouse trachea. Furthermore, the data do not support the hypothesis of atypical ETB receptors. In this preparation ET‐3 is not an ETB receptor‐selective ligand, producing contractions via activation of both ETA and ETB receptors.

British Journal of Pharmacology (2001) 132, 1905–1915; doi:10.1038/sj.bjp.0703957
Heterogeneous increases of cytoplasmic calcium: distinct effects on down‐regulation of cell surface sodium channels and sodium channel subunit mRNA levels
Authors: Shiraishi Seiji , Shibuya Izumi , Uezono Yasuhito , Yokoo Hiroki , Toyohira Yumiko , Yamamoto Ryuichi , Yanagita Toshihiko , Kobayashi Hideyuki , Wada Akihiko 
Published: January 2005

Long‐term (12 h) treatment of cultured bovine adrenal chromaffin cells with A23187 (a Ca2+ ionophore) or thapsigargin (TG) [an inhibitor of sarco(endo)plasmic reticulum Ca2+‐ATPase (SERCA)] caused a time‐ and concentration‐dependent reduction of cell surface [3H]‐saxitoxin (STX) binding capacity, but did not change the KD value. In A23187‐ or TG‐treated cells, veratridine‐induced 22Na+ influx was reduced (with no change in veratridine EC50 value) while it was enhanced by α‐scorpion venom, β‐scorpion venom, or Ptychodiscus brevis toxin‐3, like in nontreated cells.
The A23187‐ or TG‐induced decrease of [3H]‐STX binding was diminished by BAPTA‐AM. EGTA also inhibited the decreasing effect of A23187. A23187 caused a rapid, monophasic and persistent increase in intracellular concentration of Ca2+ ([Ca2+]i) to a greater extent than that observed with TG. 2,5‐Di‐(t‐butyl)‐1,4‐benzohydroquinone (DBHQ) (an inhibitor of SERCA) produced only a rapid monophasic increase in [Ca2+]i, without any effect on [3H]‐STX binding.
Reduction in [3H]‐STX binding capacity induced by A23187 or TG was attenuated by Gö6976 (an inhibitor of conventional protein kinase C) or calpastatin peptide (an inhibitor of calpain). When the internalization rate of cell surface Na+ channels was measured in the presence of brefeldin A (an inhibitor of vesicular exit from the trans‐Golgi network), A23187 or TG accelerated the reduction of [3H]‐STX binding capacity.
Six hours treatment with A23187 lowered Na+ channel α‐ and β1‐subunit mRNA levels, whereas TG had no effect.
These results suggest that elevation of [Ca2+]i caused by A23187, TG or DBHQ exerted differential effects on down‐regulation of cell surface functional Na+ channels and Na+ channel subunit mRNA levels.

British Journal of Pharmacology (2001) 132, 1455–1466; doi:10.1038/sj.bjp.0703960
Brain α2‐adrenoceptors in monoamine‐depleted rats: increased receptor density, G coupling proteins, receptor turnover and receptor mRNA
Authors: Ribas Catalina , Miralles Antonio , Busquets Xavier , García‐Sevilla Jesús A 
Published: January 2005

This study was designed to assess the molecular and cellular events involved in the up‐regulation (and receptor supersensitivity) of brain α2‐adrenoceptors as a result of chronic depletion of noradrenaline (and other monoamines) by reserpine.
Chronic reserpine (0.25 mg kg−1 s.c., every 48 h for 6 – 14 days) increased significantly the density (Bmax values) of cortical α2‐adrenoceptor agonist sites (34 – 48% for [3H]‐UK14304, 22 – 32% for [3H]‐clonidine) but not that of antagonist sites (11 – 18% for [3H]‐RX821002). Competition of [3H]‐RX821002 binding by (−)‐adrenaline further indicated that chronic reserpine was associated with up‐regulation of the high‐affinity state of α2‐adrenoceptors.
In cortical membranes of reserpine‐treated rats (0.25 mg kg−1 s.c., every 48 h for 20 days), the immunoreactivities of various G proteins (Gαi1/2, Gαi3, Gαo and Gαs) were increased (25 – 34%). Because the high‐affinity conformation of the α2‐adrenoceptor is most probably related to the complex with Gαi2 proteins, these results suggested an increase in signal transduction through α2‐adrenoceptors (and other monoamine receptors) induced by chronic reserpine.
After α2‐adrenoceptor alkylation, the analysis of receptor recovery (Bmax for [3H]‐UK14304) indicated that the increased density of cortical α2‐adrenoceptors in reserpine‐treated rats was probably due to a higher appearance rate constant of the receptor (Δr=57%) and not to a decreased disappearance rate constant (Δk=7%).
Northern‐ and dot‐blot analyses of RNA extracted from the cerebral cortex of saline‐ and reserpine‐treated rats (0.25 mg kg−1, s.c., every 48 h for 20 days) revealed that reserpine markedly increased the expression of α2a‐adrenoceptor mRNA in the brain (125%). This transcriptional activation of the receptor gene expression appears to be the cellular mechanism by which reserpine induces up‐regulation in the density of brain α2‐adrenoceptors.

British Journal of Pharmacology (2001) 132, 1467–1476; doi:10.1038/sj.bjp.0703963