bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of nitro‐L‐arginine on electrical and mechanical responses to acetylcholine in the superior mesenteric artery from stroke‐prone hypertensive rat
Authors: Ghisdal Philippe , Godfraind Théophile , Morel Nicole 
Published: January 2005

High salt diet is known to aggravate the vascular pathology in spontaneously hypertensive stroke‐prone rats (SHR‐SP). The aim of the present study was to assess the involvement of endothelial dysfunction in this effect. Contractile tension and membrane potential were simultaneously recorded in superior mesenteric artery rings of untreated and NaCl‐loaded (1% NaCl in the drinking water) SHR‐SP and normotensive Wistar Kyoto rats (WKY).
In unstimulated artery, hyperpolarization evoked by acetylcholine was not different in WKY and in NaCl‐loaded WKY; it was reduced in SHR‐SP and further reduced in NaCl‐loaded SHR‐SP. Hyperpolarization was unaffected by Nω‐nitro‐L‐arginine (L‐NA) but was abolished in high‐KCl solution.
In noradrenaline‐stimulated artery, ACh‐evoked hyperpolarization and relaxation were not different in WKY and in SHR‐SP. NaCl‐treatment did not affect the responses to ACh in WKY but decreased maximum relaxation in SHR‐SP from 93±2% to 72±7% of the contraction. In WKY, in NaCl‐loaded WKY and in SHR‐SP, L‐NA similarly shifted the concentration‐relaxation curve to ACh to the right and depressed its maximum but L‐NA did not affect the hyperpolarization to ACh. In NaCl‐loaded SHR‐SP, L‐NA blunted the effects of ACh on membrane potential and on contraction.
The NO donor SNAP abolished the depolarization and the contraction evoked by noradrenaline with the same potency in WKY and in untreated SHR‐SP but was more potent in NaCl‐loaded SHR‐SP.
In KCl‐contracted arteries the relaxations to ACh were not different in WKY and SHR‐SP but NaCl‐loaded SHR‐SP were more sensitive to ACh.
The results showed that NaCl‐rich diet markedly reduced the L‐NA‐resistant responses to ACh and increased the sensitivity to NO in SHR‐SP.

British Journal of Pharmacology (1999) 128, 1513–1523; doi:10.1038/sj.bjp.0702947
Evidence for the involvement of spinal endogenous ATP and P2X receptors in nociceptive responses caused by formalin and capsaicin in mice
Authors: Tsuda Makoto , Ueno Shinya , Inoue Kazuhide 
Published: January 2005

The aim of the present study is to characterize the role of spinal endogenous ATP and P2X receptors in the generation of neurogenic and inflammatory pain. We examined the effects of intrathecal treatment with P2X receptor antagonists on the formalin‐ and capsaicin‐induced nociceptive behaviours in mice.
Intrathecal pretreatment with the general P2 receptor antagonist, pyridoxal‐phosphate‐6‐azophenyl‐2′,4′‐disulphonic acid (PPADS), significantly suppressed both the first and second phases of the formalin‐induced nociceptive behaviour. The second phase of the nociceptive response was also suppressed by intrathecal treatment with PPADS after the first phase. Furthermore, pretreatment with the selective antagonist for the P2X1, P2X3 and P2X2+3 receptors, 2′,3′‐O‐(2,4,6‐trinitrophenyl)adenosine 5′‐triphosphate (TNP‐ATP), significantly reduced the first phase, but not the second phase. The second phase was also not suppressed by intrathecal TNP‐ATP after the first phase.
Capsaicin‐induced nociceptive behaviour that has been shown to be a model for neurogenic pain, was also significantly suppressed by intrathecal pretreatment with PPADS or TNP‐ATP.
Nociceptive behaviour in the first phase of the formalin test and in the capsaicin test were significantly inhibited by intrathecal pretreatment with α,β‐methylene ATP (α,βmeATP: 5 μg mouse−1) 15 min prior to injection of formalin or capsaicin. This treatment has been previously shown to desensitize spinal P2X3 receptor subtypes in vivo.
These findings suggest that spinal endogenous ATP may play a role in (1) the formalin‐ and capsaicin‐induced neurogenic pain via the PPADS‐ and TNP‐ATP‐sensitive P2X receptors which are also desensitized by α,βmeATP (perhaps the P2X3 receptor subtype) and (2) formalin‐induced inflammatory pain via PPADS‐sensitive, TNP‐ATP‐ and α,βmeATP‐insensitive P2X (and/or P2Y) receptors.

British Journal of Pharmacology (1999) 128, 1497–1504; doi:10.1038/sj.bjp.0702960
Characterization of excitatory prostanoid receptors in the human umbilical artery in vitro
Authors: Boersma J I , Janzen K M , Oliveira L , Crankshaw D J 
Published: January 2005

5‐HT and the prostanoid TP receptor agonists, U46619 and I‐BOP, constricted the human umbilical artery with pEC50 values of 7.3±0.2, 6.7±0.1, and 7.3±0.2, respectively. The selective TP receptor antagonist, GR32191 (0.1 μM), shifted the concentration‐effect curves to U46619 and I‐BOP to the right, but had no effect on the response to 5‐HT.
The natural prostaglandins, PGF2α and PGE2, caused concentration‐dependent contraction with pEC50 values of 5.2±0.2 and 4.9±0.2, respectively. PGD2 was a partial agonist with a pEC50 of 5.24±0.03. GR32191 (0.1 μM) inhibited the responses to all of these compounds suggesting that they produce contraction by acting at TP receptors.
Sulprostone failed to elicit contraction in the human umbilical artery at concentrations up to 4.4 μM suggesting the absence of EP1 and EP3 receptors. Despite this, 17‐phenyltrinor PGE2 and GR63799 both induced contraction at concentrations above 1 μM, but the effects were sensitive to GR32191 (0.1 μM).
Fluprostenol had no effect on the human umbilical artery at concentrations up to 17 μM suggesting the absence of FP receptors. Cloprostenol was ineffective in two tissues, but caused contraction in one tissue at the highest concentration tested (1.7 μM). However, this response was abolished in the presence of GR32191 (0.1 μM).
The effects of four TP receptor antagonists were assessed by global non‐linear regression analysis. GR32191, SQ29548, SQ30741, and ICI192605 competitively inhibited responses to U46619 with pKb values of 8.0±0.1, 7.6±0.1, 7.0±0.2 and 8.1±0.1, respectively.
These results suggest that the human umbilical artery functionally expresses TP receptors, but not EP1, EP2 or FP receptors.

British Journal of Pharmacology (1999) 128, 1505–1512; doi:10.1038/sj.bjp.0702965
A novel anti‐diabetic drug, miglitol, markedly reduces myocardial infarct size in rabbits
Authors: Minatoguchi Shinya , Arai Masazumi , Uno Yoshihiro , Kariya Tatsuya , Nishida Yoshio , Hashimoto Kazuaki , Kawasaki Masanori , Takemura Genzou , Fujiwara Takako , Fujiwara Hisayoshi 
Published: January 2005

We examined whether N‐hydroxyethyl‐1‐deoxynojirimycin (miglitol), a new human anti‐diabetic drug with effects to inhibit α‐1,6‐glucosidase glycogen debranching enzyme and reduce the glycogenolytic rate as well as to inhibit α‐1,4‐glucosidase, could reduce infarct size in the rabbit heart. Rabbits were subjected to 30‐min coronary occlusion followed by 48‐h reperfusion.
The infarct size as a percentage of area at risk was not reduced by pre‐ischaemic treatment with 1 mg kg−1 miglitol (42.7±4.0%, n=10) compared with the saline control group (41.7±2.3%, n=10). However, it was significantly and dose‐dependently reduced by pre‐ischaemic treatment with 5 or 10 mg kg−1 of miglitol (25.7±4.5%, n=10, and 14.6±2.4%, n=10, respectively) without altering the blood pressure, heart rate or blood glucose level. However, there was no evidence of an infarct‐size reducing effect after pre‐reperfusion treatment with 10 mg kg−1 of miglitol (35.0±3.0%, n=10).
Another 40 rabbits given 1, 5 and 10 mg kg−1 of miglitol or saline before ischaemia (n=10 in each) were sacrificed at 30 min of ischaemia for biochemical analysis. Miglitol preserved significantly the glycogen content, and attenuated significantly the lactate accumulation in a dose dependent manner in the ischaemic region at 30 min of ischaemia.
Pre‐ischaemic treatment, but not pre‐reperfusion treatment, with miglitol markedly reduced the myocardial infarct size, independently of blood pressure and heart rate. A dose‐dependent effect of miglitol on infarct size, glycogenolysis and lactate formation suggests that the mechanism may be related to the inhibition of glycogenolysis. Thus, miglitol may be beneficial for coronary heart disease as well as diabetes mellitus.

British Journal of Pharmacology (1999) 128, 1667–1672; doi:10.1038/sj.bjp.0702970
Nociceptin, Phe1ψ‐nociceptin1–13, nocistatin and prepronociceptin154–181 effects on calcium channel currents and a potassium current in rat locus coeruleus in vitro
Authors: Connor Mark , Vaughan Christopher W , Jennings Ernest A , Allen Richard G , Christie Macdonald J 
Published: January 2005

The actions of the neuropeptide nociceptin, the putative nociceptin receptor antagonist [Phe1ψ(CH2‐NH)Gly2]‐nociceptin‐(1–13)NH2 (Phe1ψ‐nociceptin1–13) and the putative nociceptin precursor products nocistatin (rat prepronociceptin125–132) and rat prepronociceptin154–181 were examined on membrane properties of rat locus coeruleus (LC) neurons using whole cell patch clamp techniques.
Nociceptin inhibited IBa in all LC neurons, (pD2 of 8.9, maximum inhibition 50%). The inhibition of IBa by nociceptin was associated with slowing of the activation of IBa and could be significantly reversed by a strong depolarizing prepulse. Phe1ψ‐nociceptin1–13 also inhibited IBa in LC neurons (notional pD2 of 7.6, maximum inhibition 18%). Application of Phe1ψ‐nociceptin1–13 (1 μM) significantly occluded the subsequent effects of a co‐application of nociceptin (3 nM) on IBa.
As previously reported for nociceptin, Phe1ψ‐nociceptin1–13 caused an outward current in LC neurons voltage clamped at −60 mV (pD2 of 7.1, maximum current 50% of that of methionine enkephalin, 10 μM). The Phe1ψ‐nociceptin1–13 induced current reversed polarity at −112 mV and exhibited pronounced inward rectification. Phe1ψ‐nociceptin1–13 (1 μM) reversibly inhibited the current caused by nociceptin (300 nM) by 30%.
Neither nocistatin nor rat prepronociceptin154–181 inhibited IBa in LC neurons, or prevented the subsequent inhibition by nociceptin. Neither nocistatin or prepronociceptin154–181 affected the membrane properties of LC neurons.
This study demonstrates that nociceptin modulates somatic IBa in rat LC neurons. The putative ORL1 antagonist Phe1ψ‐nociceptin1–13 exhibited partial agonist activity at inhibiting IBa and opening K+ channels in LC. Other putative nociceptin precursor products were without effect on LC cells.

British Journal of Pharmacology (1999) 128, 1779–1787; doi:10.1038/sj.bjp.0702971
CGRP and adrenomedullin binding correlates with transcript levels for Calcitonin Receptor‐Like Receptor (CRLR) and Receptor Activity Modifying Proteins (RAMPs) in rat tissues
Authors: Chakravarty P , Suthar T P , Coppock H A , Nicholl C G , Bloom S R , Legon S , Smith D M 
Published: January 2005

Putative receptors for CGRP and adrenomedullin have been investigated in the rat. Calcitonin Receptor‐Like Receptor (CRLR), in combination with Receptor Activity Modifying Proteins (RAMPs) is hypothesized to bind either CGRP or adrenomedullin. The receptors known as RDC1 and L1 have also been shown to bind CGRP and adrenomedullin respectively.
In this study it is shown that rat CRLR cDNA specifies a CGRP receptor when co‐transfected with RAMP‐1 cDNA and an adrenomedullin receptor when co‐transfected with either RAMP‐2 or RAMP‐3 cDNA in human embryonic kidney 293 cells.
CRLR, RAMP, RCD1 and L1 mRNA levels and CGRP and adrenomedullin receptor densities have been measured and correlated with each other in eight rat tissues selected for their distinctive patterns of CGRP and adrenomedullin binding.
The data are consistent with the predictions of the CRLR/RAMP model. CGRP binding correlates well with RAMP‐1 mRNA levels (R=1.0, P=0.007), adrenomedullin binding shows a tendency to vary with RAMP‐2 mRNA levels (R=0.85, P=0.14) and total binding is correlated with CRLR mRNA levels (R=0.94, P=0.03). The data do not support the hypothesis that RDC1 and L1 account for the majority of CGRP and adrenomedullin binding respectively.

British Journal of Pharmacology (2000) 130, 189–195; doi:10.1038/sj.bjp.0702975
Cardiovascular responses to angiotensins I and II in normotensive and hypertensive rats; effects of NO synthase inhibition or ET receptor antagonism
Authors: Gardiner S M , March J E , Kemp P A , Bennett T 
Published: January 2005

We compared the cardiovascular responses to angiotensins (I and II), and any possible modulatory influences thereupon of nitric oxide (NO) or endothelin (ET) in conscious male, normotensive, Hannover Sprague‐Dawley (SD) rats, and hypertensive, heterozygous ((mRen‐2)27), transgenic (TG) rats.
The pressor effects of angiotensin I or of angiotensin II were not consistently different in SD and TG rats. The accompanying absolute reductions in renal and mesenteric vascular conductances were smaller in TG rats, but probably due to the baseline vasoconstriction in those animals.
Inhibition of NO synthase with L‐NAME had no significant effects on the pressor responses to angiotensin I or angiotensin II in either SD or TG rats. L‐NAME reduced the absolute, but not percentage, reductions in renal and mesenteric vascular conductances in response to angiotensin I and angiotensin II. L‐NAME abolished the hindquarters vasodilator effects of angiotensin I and angiotensin II in both strains of rat.
ET receptor antagonism (with SB209670) had no significant influence on the pressor or renal or mesenteric vasoconstrictor effects of angiotensin II in SD rats. In TG rats, the pressor responses to angiotensin II were unaffected by SB209670; the accompanying falls in renal and mesenteric vascular conductances were enhanced in absolute, but not in percentage terms.
These results provide no evidence for a buffering action of NO, or a modulatory influence of ET, on the pressor or vasoconstrictor effects of angiotensin I and/or angiotensin II in SD rats. Furthermore, there is no evidence for an altered sensitivity to angiotensin I or angiotensin II, and no evidence for a differential modulatory influence of either NO or ET in TG, compared to SD, rats.

British Journal of Pharmacology (1999) 128, 1795–1803; doi:10.1038/sj.bjp.0702978
Effects of ω‐conotoxin GVIA and diltiazem on double peaked vasoconstrictor responses to periarterial electric nerve stimulation in isolated canine splenic artery
Authors: Yang Xiao‐Ping , Chiba Shigetoshi 
Published: January 2005

The actions of ω‐conotoxin (ω‐CTX) and diltiazem on adrenergic and purinergic components of double peaked vasoconstrictor responses to periarterial nerve stimulation have been investigated in the isolated, perfused canine splenic arterial preparation.
Double peaked vasoconstrictions (biphases of vasoconstrictors) were consistently observed in the conditions of 30 s trains of pulses at 1–10 Hz frequencies. ω‐CTX (1–30 nM) produced similar inhibitory effects on the first phase and second phase responses in a dose‐related manner. Thirty nM ω‐CTX almost completely inhibited the biphasic vasoconstrictions at any used frequencies but did not affect the vasoconstrictor responses to exogenous applied ATP (0.01–1 μmol) and noradrenaline (0.03–3 nmol).
Intraluminal application of a large dose of diltiazem (3–10 μM) also produced a dose‐dependent inhibitory effect on biphasic vasoconstrictions at any used frequencies. Three μM diltiazem exerted rather a larger inhibitory effect on the second phase than the first phase response at low frequencies (1–3 Hz), but a similar inhibition on first and second phasic responses at high frequencies (6–10 Hz). An extremely high dose of diltiazem (10 μM) almost completely inhibited the biphasic vasoconstrictor responses to nerve stimulation, and slightly inhibited the contractile responses to exogenous applied ATP (0.01–1 μmol) and noradrenaline (0.03–3 nmol).
The present results indicate that ω‐CTX selectively acts prejunctionally to inhibit the release of transmitters from sympathetic nerve terminals, and ω‐CTX‐sensitive calcium channels may produce a parallel controlling of purinergic and adrenergic components of sympathetic cotransmission. A large dose of diltiazem has inhibitory effects on both prejunctional and postjunctional sympathetic co‐transmission.

British Journal of Pharmacology (2000) 129, 47–52; doi:10.1038/sj.bjp.0702989
PF9404C, a new slow NO donor with beta receptor blocking properties
Authors: Villarroya Mercedes , Herrero Carlos J , Ruíz‐Nuño Ana , De Pascual Ricardo , Del Valle Mercedes , Michelena Pedro , Grau Manuel , Carrasco Emilio , López Manuela G , García Antonio G 
Published: January 2005

PF9404C is the S‐S diesteroisomer of a novel blocker of beta adrenergic receptors with vasodilatory properties. It causes a concentration‐dependent relaxation of rat aorta helical strips pre‐contracted with 10−6 M noradrenaline (NA; IC50 33 nM). It was equipotent to nitroglycerin (NTG; IC50 49 nM), but much more potent than isosorbide dinitrate (ISD; IC50 15,000 nM).
Oxyhaemoglobin (10 μM) shifted to the right the concentration‐response curve for the relaxation induced by PF9404C (IC50 530 nM) or NTG (IC50 61 nM).
Either methylene blue (MB) or ODQ (1 μM each) largely prevented the vasorelaxing responses to increasing concentrations of PF9404C or NTG.
In rat aorta smooth muscle cells, PF9404C increased the formation of cyclic GMP from 3 pmol mg−1 protein in basal conditions, to 53 pmol mg−1 protein in 10 μM PF9404C. Neither metoprolol nor carvedilol enhanced cyclic GMP.
In the electrically driven guinea‐pig left atrium, PF9404C blocked the inotropic effects of isoprenaline in a concentration‐dependent manner. Its IC50 (30 nM) was similar to that for S‐propranolol (22.4 nM) and lower than the IC50s for metoprolol (120 nM) and atenolol (192 nM). The beta‐adrenergic ligand (−)‐[3H]‐CGP12177 (0.2 nM) was displaced from its binding to rat brain membranes with Ki of 7 nM, 17 nM, 170 nM and 1.2 μM respectively for PF9404C, S‐(−)propranolol, metoprolol, and atenolol.
The data are consistent with the idea that the S‐S diesteroisomer PF9404C, is a potent vasorelaxing agent, as well as a blocker of cardiac beta adrenergic receptors. The mechanism of its vasorelaxing effects involves the slow generation of NO. This molecule can, therefore, exhibit antihypertensive and cardioprotective actions through a double mechanism, NO donation and beta blockade.

British Journal of Pharmacology (1999) 128, 1713–1722; doi:10.1038/sj.bjp.0702992
Effects of diadenosine polyphosphates (ApnAs) and adenosine polyphospho guanosines (ApnGs) on rat mesenteric artery P2X receptor ion channels
Authors: Lewis C J , Gitterman D P , Schlüter H , Evans R J 
Published: January 2005

Diadenosine polyphosphates (ApnAs, n=3–7) and adenosine polyphospho guanosines (ApnGs, n=3–6) are naturally occurring vasoconstrictor substances found in platelets. These vasoconstrictor actions are thought to be mediated through the activation of P2X receptors for ATP. The effects of ApnAs and ApnGs at P2X receptors on rat mesenteric arteries were determined in contraction studies and using the patch clamp technique on acutely dissociated artery smooth muscle cells.
P2X1 receptor immunoreactivity was detected in the smooth muscle layer of artery rings. The sensitivity to α,β‐methylene ATP and desensitizing nature of rat mesenteric artery P2X receptors correspond closely to those of recombinant P2X1 receptors.
Ap4A, Ap5A and Ap6A evoked concentration dependent P2X receptor inward currents which desensitized during the application of higher concentrations of agonist. The agonist order of potency was Ap5AAp6AAp4A>>Ap3A. Ap2A and Ap7A were ineffective. Similar results were obtained in contraction studies except for Ap7A which evoked a substantial contraction.
ApnGs (n=2–6)(30 μM) evoked P2X receptor inward currents in mesenteric artery smooth muscle cells. ApnGs (n=4–6) were less effective than the corresponding ApnA.
This study shows that at physiologically relevant concentrations ApnAs and ApnGs can mediate contraction of rat mesenteric arteries through the activation of P2X1‐like receptors. However the activity of the longer chain polyphosphates (n=6–7) may be overestimated in whole tissue studies due to metabolic breakdown to yield the P2X receptor agonists ATP and adenosine tetraphosphate.

British Journal of Pharmacology (2000) 129, 124–130; doi:10.1038/sj.bjp.0702993
Functional neuroimaging of cognition impaired by a classical antihistamine, d‐chlorpheniramine
Authors: Okamura Nobuyuki , Yanai Kazuhiko , Higuchi Makoto , Sakai Jun , Iwata Ren , Ido Tatsuo , Sasaki Hidetada , Watanabe Takehiko , Itoh Masatoshi 
Published: January 2005

Antihistamine induced cognitive decline was evaluated using positron emission tomography (PET) measurement of histamine H1 receptor (H1R) occupancy and regional cerebral blood flow (rCBF).
Cognitive performance in attention‐demanding task deteriorated dose‐dependently and the effects were statistically significant after the treatment of 2 mg of d‐chlorpheniramine. There was no significant change in subjective sleepiness in the same dose.
The regional blockade of H1R was observed mainly in the frontal, temporal and anterior cingulate cortices, and the intravenous administration of d‐chlorpheniramine as a therapeutic dose (2 mg) blocked over 60% of H1R in the frontal cortices.
The results from activation study using visual discrimination tasks demonstrated that enhanced activity in the right prefrontal and anterior cingulate cortices as well as a decreased activity in the left temporal and frontal cortices and midbrain after the treatment of d‐chlorpheniramine.
There were no changes in global CBF for the subjects treated with 2 mg d‐chlorpheniramine (pre; 44.8±3.3 ml dl−1 min−1 vs post; 44.4±4.7 ml dl−1 min−1).
The results indicated that the attention system of human brain could be altered by therapeutic doses of H1R antagonists. These findings provide the information as to the potential risk of antihistamines in our daily activities.

British Journal of Pharmacology (2000) 129, 115–123; doi:10.1038/sj.bjp.0702994
Adenosine induces cyclic‐AMP formation and inhibits endothelin‐1 production/secretion in guinea‐pig tracheal epithelial cells through A2B adenosine receptors
Authors: Pelletier Stéphane , Dubé Jean , Villeneuve Annie , Gobeil Fernand , Bernier Sylvie G , Battistini Bruno , Guillemette Gaétan , Sirois Pierre 
Published: January 2005

The adenosine receptor subtype mediating adenosine 3′ : 5′‐cyclic monophosphate (cyclic AMP) formation and the effect of its activation on endothelin‐1 (ET‐1) secretion were studied in primary cultures of tracheal epithelial cells.
Adenosine analogues showed the following rank order of potency (pD2 value) and intrinsic activity on the generation of cyclic AMP by tracheal epithelial cells: 5′‐N‐ethylcarboxyamidoadenosine (NECA, A1/A2A/A2B, pD2: 5.44±0.16)>adenosine (ADO, non selective, pD2: 4.99±0.09; 71±9% of NECA response) 2‐Cl‐adenosine (2CADO, non selective, pD2: 4.72±0.14; 65±9% of NECA response)>>>CGS21680 (A2A; inactive at up to 100 μM).
Cyclic AMP formation stimulated by NECA in guinea‐pig tracheal epithelial cells was inhibited by adenosine receptor antagonist with the following order of apparent affinity (pA2 value): Xanthine amine congeners (XAC, A2A/A2B, 7.89±0.22)>CGS15943 (A2A/A2B, 7.24±0.26)>ZM241385 (A2A, 6.69±0.14)>DPCPX (A1, 6.51±0.14)>3n‐propylxanthine (weak A2B, 4.30±0.10). This rank order of potency is typical for A2B‐adenosine receptor.
Adenosine decreased basal and LPS‐stimulated irET production in a concentration‐dependent manner. Moreover, NECA but not CGS21680 inhibited LPS‐induced irET production.
The inhibitory effect of NECA on LPS‐induced irET production was reversed by XAC (pA2=8.84±0.12) and DPCPX (pA2=8.10±0.22).
These results suggested that adenosine increased cyclic AMP formation and inhibited irET production/secretion by guinea‐pig tracheal epithelial cells through the activation of a functional adenosine receptor that is most likely the A2B subtype. This adenosine receptor may be involved in the regulation of the level of ET‐1 production/secretion by guinea‐pig tracheal epithelial cells in physiological as well as in pathophysiological conditions.

British Journal of Pharmacology (2000) 129, 243–250; doi:10.1038/sj.bjp.0702999