bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential effect of propofol on sympathetic neurotransmission in isolated human omental arteries and veins
Authors: Wallerstedt Susanna M , Bodelsson Mikael 
Published: January 2005

The present study was undertaken to elucidate the effect of propofol on sympathetic neurotransmission in isolated human omental vessels.
Segments of both arteries and veins were exposed to 0, 10−7, 10−6, 10−5 or 10−4 M propofol, and studied in vitro to determine effects on: (i) isometric tension after electrical field stimulation (EFS) or after exogenous administration of noradrenaline (NA); (ii) EFS‐stimulated release of [3H]‐NA from vessel segments preincubated with [3H]‐NA; (iii) uptake of [3H]‐NA.
Propofol at 10−6 M enhanced EFS‐induced contraction in artery segments, 10−7 and 10−5 M had no effect, and 10−4 M propofol depressed EFS‐induced contraction in both artery and vein segments.
Propofol did not affect the response to exogenous NA in artery and vein segments.
EFS‐stimulated release of [3H]‐NA was depressed by 10−5 and 10−4 M propofol in artery segments, and by 10−4 M in vein segments.
Uptake of [3H]‐NA was depressed by 10−6–10−4 M propofol in artery but not in vein segments.
The results suggest that sympathetic neurotransmission is enhanced at clinical concentrations (10−6 M) of propofol in human omental arteries, but not veins. This may be due to an increased availability of NA in the neuromuscular junction resulting from a reduced presynaptic reuptake. Propofol at probably supraclinical concentrations (10−5–10−4 M) impairs the sympathetic neurotransmission in both human omental arteries and veins, probably due to an inhibitory effect on the NA release from the sympathetic nerves.

British Journal of Pharmacology (1998) 125, 120–126; doi:10.1038/sj.bjp.0702021
Assessment of the effect of malaria infection on hepatic clearance of dihydroartemisinin using rat liver perfusions and microsomes
Authors: Batty Kevin T , Ilett Kenneth F , Edwards Geoffrey , Powell Shane M , Maggs James L , Park B Kevin , Davis Timothy M E 
Published: January 2005

The clearance of dihydroartemisinin (DHA) in control and malaria‐infected (MI) rats was investigated using the isolated perfused rat liver (IPRL) model and hepatic microsomal studies.
In the recirculating IPRL, clearance of DHA was reduced from a mean (s.d.) of 8.2±1.8 ml min−1 in controls (n=8) to 6.0±1.0 ml min−1 in MI (n=8; P<0.01). Clearance in control livers was similar to the perfusion flow rate, suggesting a high hepatic extraction ratio for DHA.
Single‐pass IPRL studies in controls (n=8) showed that DHA bioavailability at 1.3, 8 and 38 μM was 0.026±0.020, 0.043±0.025 and 0.14±0.06, respectively (P<0.001 for 8 μM vs 38 μM). In MI livers (n=5), DHA bioavailability at 8 and 38 μM was 0.18±0.07 and 0.40±0.08, respectively (P=0.002). Bioavailability was higher in the MI group than in controls (P=0.01 at 8 μM and P<0.001 at 38 μM). DHA‐glucuronide was the sole biliary metabolite.
Hepatic microsomal studies of DHA‐glucuronide formation showed a significantly lower Vmax, but no significant change in Km, in MI compared to control livers (n=6). Intrinsic metabolic clearance (Vmax/Km) was higher in control than in MI livers (5.2±1.3 and 2.5±1.4 μl min−1 mg−1, respectively; P=0.006).
These studies demonstrate that DHA has a high, concentration‐dependent hepatic extraction ratio that is reduced by 20–30% in the P. berghei rodent malaria model. The impaired hepatic clearance of DHA in MI is attributable to a reduction in intrinsic metabolic clearance.

British Journal of Pharmacology (1998) 125, 159–167; doi:10.1038/sj.bjp.0702023
Influence of various combinations of specific antibody dose and affinity on tissue imipramine redistribution
Authors: Ragusi Corinne , Boschi Gabrielle , Risède Patricia , Rips Richard , Harrison Kenneth , Scherrmann Jean‐Michel 
Published: January 2005

This study was designed to evaluate the distribution kinetics of imipramine (Imip) in the brain and the main peripheral organs (heart, kidney, liver and lung) of rats, and to establish the relationship between the redistribution of Imip from these tissues and the immunoreactive capacity (dose and affinity) of anti‐TCA IgG.
[3H]‐Imip (1 nmol kg−1 body weight) was injected intravenously 6 min before the i.v. injection of antibodies. At this time, the concentrations of Imip and its main metabolites in plasma were determined. The radioactivity measured corresponded to 91.7% Imip, indicating that the pharmacokinetics reflected essentially Imip. Plasma and tissue Imip contents were measured over the interval 1 to 90 min in control and in treated rats. The antibodies used were a murine monoclonal IgG1 (Ka=3.8 107 M−1) at an IgG1/Imip molar ratio of 1000 (IgG1 1000), and a sheep polyclonal IgG (TAb, Ka=1.3 1010 M−1) at IgG/Imip molar ratios of 1, 10 and 100 (TAb1, TAb10 and TAb100).
The anti‐TCA IgG increased the plasma [3H]‐Imip concentrations: the AUC1→60 min for [3H]‐Imip were 4 (IgG1 1000), 9 (TAb1), 33.9 (TAb10) and 41.4 (TAb100) times higher in the treated groups than in the controls. The opposite effect occurred in the brain, heart and lungs, with large, rapid decreases in Imip. The increase in plasma Imip and the decrease in tissue Imip depended on the immunoreactive capacity (NKa) of the antibody, where N=molar concentration of IgG binding sites and Ka=IgG affinity constant. Maximal plasma and tissue redistribution occurred when NKa=33.8×104.
Imip redistribution can be controlled using various doses or affinities of specific antibodies, and the resulting rapid, extensive Imip redistribution from the main target organs could be very promising for TCA detoxification.

British Journal of Pharmacology (1998) 125, 35–40; doi:10.1038/sj.bjp.0702033
Potent vasodilatory with minor cardiodepressant actions of mibefradil in human cardiac tissue
Authors: Brixius Klara , Mohr Valeska , Müller‐Ehmsen Jochen , Hoischen Susanne , Münch Götz , Schwinger Robert H G 
Published: January 2005

The present study compared the cardiovascular effects of mibefradil (MIB), a novel Ca2+‐channel antagonist with high selectivity for T‐type Ca2+‐channels to the effect of the L‐type Ca2+‐channel‐antagonists nifedipine (NIF) and diltiazem (DIL) in left ventricular myocardium and coronary arteries of hearts obtained from patients suffering from dilated cardiomyopathy (NYHA IV). Right atrial myocardium from patients undergoing aortocoronary bypass surgery without signs of cardiac failure was studied as well.
NIF and DIL (100 μmol l−1) completely depressed force of contraction (FOC) in electrically driven left ventricular myocardium (NIF 6.5±1.4% and DIL 7.1±1.2% of control), whereas a similar concentration of MIB only reduced force of contraction to 55.1±4.0% of the basal FOC. The negative inotropic potency as measured by the concentration needed to reduce basal FOC for 25% was NIF (0.0095 μmol l−1)>DIL (0.041 μmol l−1)>MIB (9.47 μmol l−1).
All three Ca2+‐channel antagonists were more potent in human atrial compared to human left ventricular myocardium to reduce FOC.
The rank order of Ca2+‐antagonistic moiety as measured by the decrease of the intracellular Ca2+‐transient (fura‐2 ratio method) was NIF>DIL>MIB.
All Ca2+‐channel antagonists completely relaxed human coronary arteries (% of papaverine effect: MIB 81.7±5.5%, DIL 91.3±0.9%, NIF 96.4±3.7%) precontracted with PGF2α (0.3 μmol l−1). The rank order of vasodilatory potency was NIF (EC50; 0.02 μmol l−1)>DIL (0.13 μmol l−1)>MIB (2.05 μmol l−1).
The vasoselectivity measured by the ratio of the concentration needed to achieve a 25% decrease in force and the concentration needed for 25% vasodilatation was 316 for MIB, 1.5 for NIF and 1.0 for DIL.
The present study provides evidence that blockade of T‐type Ca2+‐channels (e.g. mibefradil) results in potent vasodilatory properties with only minor cardiodepressant effects.

British Journal of Pharmacology (1998) 125, 41–48; doi:10.1038/sj.bjp.0702034
Pharmacological characterization of a rat 5‐hydroxytryptamine type3 receptor subunit (r5‐HT3A(b)) expressed in Xenopus laevis oocytes
Authors: Mair Ian D , Lambert Jeremy J , Yang Jay , Dempster John , Peters John A 
Published: January 2005

The present study has utilized the two electrode voltage‐clamp technique to examine the pharmacological profile of a splice variant of the rat orthologue of the 5‐hydroxytryptamine type 3A subunit (5‐HT3A(b)) heterologously expressed in Xenopus laevis oocytes.
At negative holding potentials, bath applied 5‐HT (300 nM–10 μM) evoked a transient, concentration‐dependent (EC50=1.1±0.1 μM), inward current. The response reversed in sign at a holding potential of −2.1±1.6 mV.
The response to 5‐HT was mimicked by the 5‐HT3 receptor selective agonists 2‐methyl‐5‐HT (EC50=4.1±0.2 μM), 1‐phenylbiguanide (EC50=3.0±0.1 μM), 3‐chlorophenylbiguanide (EC50=140± 10 nM), 3,5‐dichlorophenylbiguanide (EC50=14.5±0.4 nM) and 2,5‐dichlorophenylbiguanide (EC50= 10.2±0.6 nM). With the exception of 2‐methyl‐5‐HT, all of the agonists tested elicited maximal current responses comparable to those produced by a saturating concentration (10 μM) of 5‐HT.
Responses evoked by 5‐HT at EC50 were blocked by the 5‐HT3 receptor selective antagonist ondansetron (IC50=231±22 pM) and by the less selective agents (+)‐tubocurarine (IC50=31.9± 0.01 nM) and cocaine (IC50=2.1±0.2 μM).
The data are discussed in the context of results previously obtained with the human and mouse orthologues of the 5‐HT3A subunit. Overall, the study reinforces the conclusion that species differences detected for native 5‐HT3 receptors extend to, and appear largely explained by, differences in the properties of homo‐oligomeric receptors formed from 5‐HT3A subunit orthologues.

British Journal of Pharmacology (1998) 124, 1667–1674; doi:10.1038/sj.bjp.0702037
Suppression of macrophage inflammatory protein (MIP)‐1α production and collagen‐induced arthritis by adenosine receptor agonists
Authors: Szabó Csaba , Scott Gwen S , Virág László , Egnaczyk Greg , Salzman Andrew L , Shanley Thomas P , Haskó György 
Published: January 2005

Ligands of the various adenosine receptor subtypes modulate the production of pro‐and anti‐inflammatory cytokines. Here we evaluated the effect of adenosine and various ligands of the adenosine receptor subtypes (A1, A2, A3) on the chemokine macrophage inflammatory protein (MIP) 1α production in immunostimulated RAW macrophages in vitro. Furthermore, we studied whether a selected A3 adenosine receptor agonist inhibits MIP‐1α production and affects the course of inflammation in collagen‐induced arthritis.
In the cultured macrophages, the A3 receptor agonist N6‐(3‐iodobenzyl)‐adenosine‐5′‐N‐methyluronamide (IB‐MECA), and, less potently, the A2 receptor agonist 2‐p‐(2‐carboxyethyl) phenethylamino‐5′‐N‐ethyl‐carboxamidoadenosine (CGS; 1–200 μM) dose‐dependently suppressed the production of MIP‐1α. The selective A1 receptor agonist 2‐chloro‐N6‐cyclopentyladenosine (CCPA, 1–200 μM) was ineffective, and adenosine was a weak inhibitor. The inhibition of MIP‐1α production by the A3 and A2 agonist was associated with suppression of its steady‐state mRNA levels.
Based on the in vitro data, we concluded that activation of A3, and to a lesser extent A2 adenosine receptors suppresses MIP‐1α expression. Since IB‐MECA was the most potent inhibitor of MIP‐1α expression, we next investigated whether it affects the production of other pro‐inflammatory mediators. We observed that IB‐MECA (1–300 μM) inhibited, in a dose‐dependent manner, the production of IL‐12, IL‐6, and, to a lesser extent, nitric oxide in the immunostimulated cultured macrophages.
Since MIP‐α is a chemokine which enhances neutrophil recruitment into inflammatory sites, we investigated whether the A3 agonist IB‐MECA affects the course of inflammation, MIP‐α production and the degree of neutrophil recruitment in arthritis. In a model of collagen‐induced arthritis in mice, IB‐MECA (0.5 mg/kg/day) reduced the severity of joint inflammation. IB‐MECA inhibited the formation of MIP‐1α, IL‐12 and nitrotyrosine (an indicator of reactive nitrogen species) in the paws, and suppressed neutrophil infiltration.
We conclude that adenosine receptor agonists, most notably the A3 agonist IB‐MECA suppress the production of MIP‐α, and exert anti‐inflammatory effects. Therefore, stimulation of adenosine receptor subtypes A3 and A2 may be a strategy worthy of further evaluation for the abrogation of acute or chronic inflammatory disorders.

British Journal of Pharmacology (1998) 125, 379–387; doi:10.1038/sj.bjp.0702040
Evidence that S‐adenosyl‐L‐methionine diastereoisomers may reduce ischaemia‐reperfusion injury by interacting with purinoceptors in isolated rat liver
Authors: Dunne J Bruce , Alexander Barry , Williams Roger , Tredger J Michael 
Published: January 2005

Mechanisms underlying the haemodynamic activity of diastereoisomers of S‐adenosyl‐L‐methionine (SAM) were investigated using inhibitors of purinoceptors and nitric oxide (NO) synthase in perfused rat livers damaged by sequential 24 h cold and 20 min rewarming ischaemia+reperfusion.
Stored livers were flushed with 10 ml saline alone (control) or with added (R,S) or (S,S) SAM (100 μM) and reperfused in the absence (control) or presence of 10 μM 8‐phenyltheophylline (8‐PT) or 100 μM L‐N‐monomethylarginine (L‐NMMA).
Both SAM diastereoisomers rapidly increased blood flow and bile production versus controls (P<0.001) but the (R,S) isomer induced greater increases in blood flow and the (S,S) isomer greater increases in bile production: 625 versus 596 versus 518 ml blood flow and 100 versus 119 versus 56 mg bile production per g liver over 3 h in (R,S), (S,S) and control, respectively.
8‐PT prevented the enhancement of blood flow by (S,S) SAM (529 versus 596 ml g −1liver over 3 h for (S,S) SAM alone, P<0.001), but was without effect in control livers. 8‐PT also reduced SAM‐enhanced bile production: 51 versus 119 mg g −1liver over 3 h, P<0.001. L‐NMMA reduced blood flow and bile production similarly in the absence or presence of (S,S) SAM.
Thus, SAM may improve liver perfusion after ischaemia‐reperfusion injury via stimulation of P1 (A2) purinoceptors at which SAM shows activity. The choleretic activity of (S,S) SAM is disproportionately greater than enhanced blood flow and may occur independently of a NO‐dependent component of bile production.

British Journal of Pharmacology (1998) 125, 225–233; doi:10.1038/sj.bjp.0702043
Human vascular to cardiac tissue selectivity of L‐ and T‐type calcium channel antagonists
Authors: Sarsero Doreen , Fujiwara Toshimasa , Molenaar Peter , Angus James A 
Published: January 2005

Voltage‐operated calcium channel (VOCC) antagonists are effective antihypertensive and antianginal agents but they also depress myocardial contractility.
We compared four L‐type calcium channel antagonists, felodipine, nifedipine, amlodipine and verapamil and a relatively T‐type selective calcium channel antagonist, mibefradil, on human and rat isolated tissue assays to determine their functional vascular to cardiac tissue selectivity (V/C) ratio.
The V/C ratio was calculated as the ratio of the IC50 value of the antagonist that reduced (by 50%) submaximally contracted (K+ 62 mM) human small arteries from the aortic vasa vasorum (vascular, V) mounted in a myograph and the IC50 value of the antagonist that reduced (−)‐isoprenaline (6 nM) submaximally stimulated human right atrial trabeculae muscle (cardiac, C) mounted in organ chambers.
The average pIC50 values (−log IC50 M) for the human vascular preparations were felodipine 8.30, nifedipine 7.78, amlodipine 6.64, verapamil 6.26 and mibefradil 6.22. The average pIC50 values for the cardiac muscle were felodipine 7.21, nifedipine 6.95, verapamil 6.91, amlodipine 5.94, and mibefradil 4.61.
The V/C ratio calculated as antilog [pIC50V‐pIC50C] is thus mibefradil 41, felodipine 12, nifedipine 7, amlodipine 5 and verapamil 0.2.
In rat small mesenteric arteries the pIC50 values for the five drugs were similar to the values for human vasa vasorum arteries contracted by K+ 62 mM. However for methoxamine (10 μM) contraction in the rat arteries the pIC50 values were lower for felodipine 7.24 and nifedipine 6.23, but similar for verapamil 6.13, amlodipine 6.28 and mibefradil 5.91.
In conclusion, in the human tissue assays, the putative T‐channel antagonist mibefradil shows the highest vascular to cardiac selectivity ratio; some 3 fold higher than the dihydropyridine, felodipine, and some 200 fold more vascular selective than the phenylalkylamine, verapamil. This favourable vascular to cardiac selectivity for mibefradil, from a new chemical class of VOCC antagonist, may be explained by its putative T‐channel selectivity.

British Journal of Pharmacology (1998) 125, 109–119; doi:10.1038/sj.bjp.0702045
Fading and rebound of P2X2 currents at millimolar ATP concentrations caused by low pH
Authors: Stoop R , Quayle J M 
Published: January 2005

When ATP is applied at high concentrations (above 1 mM) to PC12 cells, it produces a rapidly desensitizing peak current followed by a rebound of the current after termination of the ATP application. We expressed P2X2 receptors, which are thought to mediate the ATP currents of PC12 cells, in HEK293 cells and studied the effects of acidification on this ‘fading and rebound’ phenomenon. We found that the desensitization disappeared after adjusting the low pH (<5.0) of the millimolar ATP concentrations to a more physiological value (pH 7.3). Furthermore, the fading and rebound could also be induced at much lower ATP concentrations by decreasing the pH of the ATP containing application solutions. Thus, it appears this phenomenon is not caused directly by high concentrations of ATP, but is due to a concomitant acidification that occurs when high concentrations of ATP are dissolved in only moderately buffered application solutions.British Journal of Pharmacology (1998) 125, 235–237; doi:10.1038/sj.bjp.0702056
Calcitonin gene‐related peptide potentiates nicotinic acetylcholine receptor‐operated slow Ca2+ mobilization at mouse muscle endplates
Authors: Salim Safaa Y , Dezaki Katsuya , Tsuneki Hiroshi , Abdel‐Zaher Ahmed O , Kimura Ikuko 
Published: January 2005

The involvement of calcitonin gene‐related peptide (CGRP) in the non‐contractile slow Ca2+ mobilization induced by prolonged nicotinic stimulation was investigated by measurement of [Ca2+]i levels in mouse single muscle cells (flexor digitorum brevis; FDB) loaded with a Ca2+ indicator fluo‐3 using confocal laser scanning microscopy.
CGRP (3–30 nM) potentiated acetylcholine (ACh, 1 μM)‐elicited slow Ca2+ mobilization in a concentration‐dependent manner.
The potentiation by CGRP of the slow Ca2+ component was greatly depressed by a competitive nicotinic antagonist (+)‐tubocurarine (5 μM). The Ca2+ channel blocker nitrendipine (1 μM) affected neither ACh responses nor the CGRP potentiation.
The slow Ca2+ component was completely abolished by reducing [Ca2+]0 from 2.5 to 0.25 mM whereas the fast component was not affected. The CGRP‐induced potentiation of slow Ca2+ signal was also depressed by decreasing [Ca2+]0.
Isoproterenol (30 μM) and 8‐bromo‐adenosine 3′,5′‐cyclic monophosphate (1 mM) potentiated the ACh‐elicited slow Ca2+ response. The potentiation by CGRP of the slow Ca2+ component was completely abolished by a protein kinase‐A inhibitor H‐89 (1 μM).
These findings indicate that CGRP potentiates the nicotinic ACh receptor‐operated slow Ca2+ signal via the activation of protein kinase‐A system at the skeletal muscle endplates.

British Journal of Pharmacology (1998) 125, 277–282; doi:10.1038/sj.bjp.0702058
SB‐224289–a novel selective (human) 5‐HT1B receptor antagonist with negative intrinsic activity
Authors: Selkirk J V , Scott C , Ho M , Burton M J , Watson J , Gaster L M , Collin L , Jones B J , Middlemiss D N , Price G W 
Published: January 2005

Human 5‐HT1B (h5‐HT1B) and human 5‐HT1D (h5‐HT1D) receptors show remarkably similar pharmacology with few compounds discriminating the receptors. We report here on a novel compound, SB‐224289 (1′‐Methyl‐5‐[[2′‐methyl‐4′‐(5‐methyl‐1,2,4‐oxadiazol‐3‐yl)biphenyl‐4‐yl]carbonyl]‐2,3,6,7‐tetrahydrospiro [furo [2,3‐f]indole‐3,4′‐piperidine] oxalate), which has high affinity for h5‐HT1B receptors (pK1=8.16±0.06) and displays over 75 fold selectivity for the h5‐HT1B receptor over all other 5‐HT receptors including the h5‐HT1D receptor and all other receptors tested thus far.
Functional activity of SB‐224289 was measured in a [35S]GTPγS binding assay on recombinant h5‐HT1B and h5‐HT1D receptors expressed in Chinese Hamster Ovary (CHO) cells. SB‐224289 displayed negative intrinsic activity at both receptors with higher potency at h5‐HT1B receptors. SB‐224289 caused a rightward shift of agonist concentration response curves consistent with competitive antagonism and generated affinities comparable with those obtained from competition radioligand receptor binding studies.
SB‐224289 potentiated [3H]5‐HT release from electrically stimulated guinea‐pig cerebral cortical slices to the same extent as as the non‐selective 5‐HT1 antagonist methiothepin. SB‐224289 also fully reversed the inhibitory effect of exogenously superfused 5‐HT on electrically stimulated release.
Using SB‐224289 as a tool compound, we confirm that in guinea‐pig cerebral cortex the terminal 5‐HT autoreceptor is of the 5‐HT1B subtype.

British Journal of Pharmacology (1998) 125, 202–208; doi:10.1038/sj.bjp.0702059
Molecular cloning and functional characterization of a rat somatostatin sst2(b) receptor splice variant
Authors: Schindler Marcus , Kidd Emma J , Carruthers Alan M , Wyatt Mark A , Jarvie Emma M , Sellers Lynda A , Feniuk Wasyl , Humphrey Patrick P A 
Published: January 2005

The mouse somatostatin (SRIF) sst2 receptor exists in two splice variants, sst2(a) and sst2(b), which differ in their intracellular carboxy‐termini only. The murine sst2(b) receptor was reported to be less prone to agonist‐induced desensitization as compared with the sst2(a) receptor. To determine whether a sst2(b) splice variant with similar functional characteristics exists in the rat, we have isolated a cDNA fragment from rat gastric mucosa encoding a sst2(b) receptor and expressed the full‐length protein in CHO‐K1 cells for functional characterization.
This study provides the first evidence for the occurrence in the rat of the sst2(b) receptor, which has a 15 amino acid carboxy‐terminus differing in composition to the 38 amino acid C‐terminus of the rat sst2(a) receptor.
In CHO‐K1 cells expressing rat recombinant sst2(a) or sst2(b) receptors, SRIF caused concentration‐dependent increases in extracellular acidification rates (EAR) with pEC50 values of 9.0 and 9.9, respectively. Pre‐treatment with pertussis toxin (Ptx) caused a rightward displacement of the SRIF concentration‐effect curves with pEC50 values of 8.3 (sst2(a)) and 8.4 (sst2(b)).
SRIF (3 pM–3 nM) also caused concentration‐dependent inhibition of forskolin‐stimulated cyclic AMP formation in CHO‐sst2(a) cells (pIC50 10.5) and CHO‐sst2(b) cells (pIC50 10.4). The degree of inhibition was less with higher concentrations of SRIF resulting in bell‐shaped concentration‐effect curves. Following pre‐treatment with Ptx, the inhibitory effect of SRIF was abolished and SRIF caused only increases in cyclic AMP formation.
Both the SRIF‐induced increases in EAR and inhibition of cyclic AMP formation were susceptible to agonist‐induced desensitization, but this was less apparent following pre‐treatment with Ptx.
This demonstrates that the operational characteristics of the recombinant rat sst2(a) and sst2(b) receptors are broadly similar. Both isoforms couple to Ptx‐sensitive as well as ‐insensitive G proteins and are equally prone to agonist‐induced desensitization.

British Journal of Pharmacology (1998) 125, 209–217; doi:10.1038/sj.bjp.0702064