bluuebunny/crossref_metadata_2025_split huggingface dataset:
The phosphatidylinositol 4‐kinase inhibitor phenylarsine oxide blocks evoked neurotransmitter release by reducing calcium entry through N‐type calcium channels
Authors: Searl T J , Silinsky E M 
Published: January 2005

The effects of the phosphatidylinositol 4‐kinase inhibitor, phenylarsine oxide (PAO), on acetylcholine (ACh) release and on prejunctional Ca2+ currents were studied at the frog neuromuscular junction using electrophysiological recording techniques.
Application of PAO (30 μM) increased both spontaneous ACh release reflected as miniature end‐plate potential (mepp) frequencies and evoked ACh release reflected as end‐plate potential (epp) amplitudes with a similar time course.
Following the initial increase in epp amplitudes produced by PAO, epps slowly declined and were eventually abolished after approximately 20 min. However, mepp frequencies remained elevated over this time period.
PAO (30 μM) also inhibited the perineural voltage change associated with Ca2+ currents through N‐type Ca2+ channels (prejunctional Ca2+ currents) at motor nerve endings. Addition of British anti‐lewisite (BAL, 1 mM), an inactivator of PAO, partially reversed both the inhibition of epps and the inhibition of the prejunctional Ca2+ current.
The effects of PAO on N‐type Ca2+ channels were investigated more directly using the whole cell patch clamp technique on acutely dissociated sympathetic neurons. Application of PAO (30–40 μM) to these neurons decreased the voltage‐activated calcium currents through N‐type Ca2+ channels, an effect that was partially reversible by BAL.
In combination, these results suggest that inhibition of neurotransmitter release by PAO occurs as a consequence of the inhibition of Ca2+ entry via N‐type calcium channels. The relationship between the effects of PAO on N‐type Ca2+ channels in motor nerve endings and in neuronal soma is discussed.

British Journal of Pharmacology (2000) 130, 418–424; doi:10.1038/sj.bjp.0703299
Evidence for a M1 muscarinic receptor on the endothelium of human pulmonary veins
Authors: Walch Laurence , Gascard Jean‐Pierre , Dulmet Elisabeth , Brink Charles , Norel Xavier 
Published: January 2005

To characterize the muscarinic receptors on human pulmonary veins associated with the acetylcholine (ACh)‐induced relaxation, isolated venous and arterial preparations were pre‐contracted with noradrenaline (10 μM) and were subsequently challenged with ACh in the absence or presence of selective muscarinic antagonists.
ACh relaxed venous preparations derived from human lung with a pD2 value of 5.82±0.09 (n=16). In venous preparations where the endothelium had been removed, the ACh relaxations were abolished (n=4). ACh relaxed arterial preparations with a pD2 value of 7.06±0.14 (n=5).
Atropine (1 μM), the non selective antagonist for muscarinic receptors, inhibited ACh‐induced relaxations in human pulmonary veins. The affinity value (pKB value) for atropine was: 8.64±0.10 (n=5). The selective muscarinic antagonists (darifenacin (M3), himbacine (M2,M4), methoctramine (M2) and pFHHSiD (M1,M3)) also inhibited ACh‐induced relaxations in venous preparations. The pKB values obtained for these antagonists were not those predicted for the involvement of M2–5 receptors in the ACh‐induced relaxation in human pulmonary veins.
The pKB value for darifenacin (1 μM) was significantly greater in human pulmonary arterial (8.63±0.14) than in venous (7.41±0.20) preparations derived from three lung samples.
In human pulmonary veins, the pKB values for pirenzepine (0.5 and 1 μM), a selective antagonist for M1 receptors, were: 7.89±0.24 (n=7) and 8.18±0.22 (n=5), respectively. In the venous preparations, the pKB values derived from the functional studies with all the different muscarinic antagonists used were correlated (r=0.89; P=0.04; slope=0.78) with the affinity values (pKi values) previously published for human cloned m1 receptors in CHO cells.
These results suggest that the relaxations induced by ACh are due to the activation of M1 receptors on endothelial cells in isolated human pulmonary veins.

British Journal of Pharmacology (2000) 130, 73–78; doi:10.1038/sj.bjp.0703301
Modulation of 3H‐noradrenaline release by presynaptic opioid, cannabinoid and bradykinin receptors and β‐adrenoceptors in mouse tissues
Authors: Trendelenburg A U , Cox S L , Schelb V , Klebroff W , Khairallah L , Starke K 
Published: January 2005

Release‐modulating opioid and cannabinoid (CB) receptors, β‐adrenoceptors and bradykinin receptors at noradrenergic axons were studied in mouse tissues (occipito‐parietal cortex, heart atria, vas deferens and spleen) preincubated with 3H‐noradrenaline.
Experiments using the OP1 receptor‐selective agonists DPDPE and DSLET, the OP2‐selective agonists U50488H and U69593, the OP3‐selective agonist DAMGO, the ORL1 receptor‐selective agonist nociceptin, and a number of selective antagonists showed that the noradrenergic axons innervating the occipito‐parietal cortex possess release‐inhibiting OP3 and ORL1 receptors, those innervating atria OP1, ORL1 and possibly OP3 receptors, and those innervating the vas deferens all four opioid receptor types.
Experiments using the non‐selective CB agonists WIN 55,212‐2 and CP 55,940 and the CB1‐selective antagonist SR 141716A indicated that the noradrenergic axons of the vas deferens possess release‐inhibiting CB1 receptors. Presynaptic CB receptors were not found in the occipito‐parietal cortex, in atria or in the spleen.
Experiments using the non‐selective β‐adrenoceptor agonist isoprenaline and the β2‐selective agonist salbutamol, as well as subtype‐selective antagonists, demonstrated the occurrence of release‐enhancing β2‐adrenoceptors at the sympathetic axons of atria and the spleen, but demonstrated their absence in the occipito‐parietal cortex and the vas deferens.
Experiments with bradykinin and the B2‐selective antagonist Hoe 140 showed the operation of release‐enhancing B2 receptors at the sympathetic axons of atria, the vas deferens and the spleen, but showed their absence in the occipito‐parietal cortex.
The experiments document a number of new presynaptic receptor locations. They confirm and extend the existence of marked tissue and species differences in presynaptic receptors at noradrenergic neurons.

British Journal of Pharmacology (2000) 130, 321–330; doi:10.1038/sj.bjp.0703305
Induced desensitization of the insulinotropic effects of antidiabetic drugs, BTS 67 582 and tolbutamide
Authors: McClenaghan Neville H , Ball Andrew J , Flatt Peter R 
Published: January 2005

Acute and chronic mechanisms of action of novel insulinotropic antidiabetic drug, BTS 67 582 (1,1‐dimethyl‐2‐(2‐morpholinophenyl)guanidine fumarate), were examined in the stable cultured BRIN‐BD11 cell line.
BTS 67 582 (100–400 μM) stimulated a concentration‐dependent increase (P<0.01) in insulin release at both non‐stimulatory (1.1 mM) and stimulatory (8.4 mM) glucose.
Long‐term exposure (3–18 h) to 100 μM BTS 67 582 in culture time‐dependently decreased subsequent responsiveness to acute challenge with 200 μM BTS 67 582 or 200 μM tolbutamide at 12–18 h (P<0.001). Similarly 3–18 h culture with the sulphonylurea, tolbutamide (100 μM), also effectively suppressed subsequent insulinotropic responses to both BTS 67 582 and tolbutamide.
Culture with 100 μM BTS 67 582 or 100 μM tolbutamide did not affect basal insulin secretion, cellular insulin content, or cell viability and exerted no influence on the secretory responsiveness to 200 μM of the imidazoline, efaroxan.
While 18 h BTS 67 582 culture did not affect the insulin‐releasing actions (P<0.001) of 16.7 mM glucose, 10 mM arginine, 30 mM KCl, 25 μM forskolin or 10 nM phorbol‐12‐myristate 13‐acetate (PMA), significant inhibition (P<0.001) of the insulinotropic effects of 10 mM 2‐ketoisocaproic acid (KIC) and 10 mM alanine were observed.
These data suggest that BTS 67 582 shares a common signalling pathway to sulphonylurea but not imidazoline drugs. Desensitization of drug action may provide an important approach to dissect sites of action of novel and established insulinotropic antidiabetic agents.

British Journal of Pharmacology (2000) 130, 478–484; doi:10.1038/sj.bjp.0703306
Protective effects of Cyclosporin‐A in splanchnic artery occlusion shock
Authors: Squadrito Francesco , Altavilla Domenica , Squadrito Giovanni , Ferlito Marcella , Deodato Barbara , Arlotta Mariarita , Minutoli Letteria , Campo Giuseppe M , Bova Antonio , Quartarone Cristina , Urna Giuseppe , Sardella Aurora , Saitta Antonino , Caputi Achille P 
Published: January 2005

Cyclosporin A (CsA) is an immunosuppressant drug that inhibits nitric oxide (NO) synthase induction in vascular smooth muscle cells. Splanchnic artery occlusion (SAO) shock is a lethal type of shock characterized by a marked vascular dysfunction in which the L‐arginine/nitric oxide pathway plays an important role. We investigated whether CsA exerts protective effects in SAO shock by interfering with the L‐arginine/nitric oxide pathway.
Male anaesthetized rats (n=156) were subjected to clamping of the splanchnic arteries for 45 min. This surgical procedure resulted in an irreversible state of shock (SAO shock). Sham operated animals were used as controls. SAO shocked rats had a decreased survival (86±6 min, while sham shocked rats survived more than 240 min), marked hypotension, increased serum levels of TNF‐α, enhanced plasma nitrite/nitrate concentrations (75±7.1 μM; sham shocked rats=1.6±0.5 μM) and enhanced inducible NO synthase (iNOS) protein induction and activity in the aorta. Moreover aortic rings from shocked rats showed a marked hyporeactivity to phenylephrine (PE, 1 nM–10 μM).
CsA (0.25, 0.5 and 1 mg kg−1, 5 min after reperfusion) increased survival rate (SAO+CsA=236±9 min following the highest dose), reverted the marked hypotension, reduced plasma nitrite/nitrate concentration (11±5.2 μM following the highest dose), restored to control values the hyporeactivity to PE, and blunted iNOS protein induction and activity in aortic rings.
The present data indicate that in an experimental rat model CsA may have antishock properties related to inhibition of L‐arginine/nitric oxide pathway.

British Journal of Pharmacology (2000) 130, 339–344; doi:10.1038/sj.bjp.0703310
Heat stress‐induced protection of endothelial function against ischaemic injury is abolished by ATP‐sensitive potassium channel blockade in the isolated rat heart
Authors: Joyeux Marie , Bouchard Jean‐François , Lamontagne Daniel , Godin‐Ribuot Diane , Ribuot Christophe 
Published: January 2005

The protection conferred by heat stress (HS) against myocardial ischaemia‐reperfusion injury, in terms of mechanical function preservation and infarct size reduction, is well documented and mechanisms underlying these effects have been extensively explored. However, the effect of HS on coronary circulation is less known. The aim of this study was thus to investigate the role of ATP‐sensitive potassium (KATP) channels in the protection against ischaemic injury afforded by HS to the coronary endothelial function.
Twenty‐four hours after whole body hyperthermia (42°C for 15 min, H groups) or sham anaesthesia (Sham groups), isolated perfused rat hearts were subjected to a 15 min stabilization period followed by a 30 min infusion of either 0.3 μM glibenclamide (Gli, a KATP channel blocker) or its vehicle (V). Hearts were then exposed to a low‐flow ischaemia (30 min)‐reperfusion (20 min) (I/R) or normally perfused (50 min), after which coronaries were precontracted with 0.1 μM U‐46619. Finally, the response to the endothelium‐dependent vasodilator, 5‐hydroxytryptamine (5‐HT, 10 μM) was compared to that of the endothelium‐independent vasodilator, sodium nitroprusside (SNP, 3 μM).
In hearts from Sham‐V and Sham‐Gli groups, I/R selectively diminished 5‐HT‐induced vasodilatation without affecting the vasodilatation to SNP. In V‐treated groups, prior HS preserved the vasodilatation produced by 5‐HT. This HS‐induced protection was abolished by Gli treatment.
In conclusion, these results suggest that KATP channel activation contributes to the preservation of coronary endothelial function conferred by heat stress against ischaemic insult.

British Journal of Pharmacology (2000) 130, 345–350; doi:10.1038/sj.bjp.0703312
Contractile responses to human urotensin‐II in rat and human pulmonary arteries: effect of endothelial factors and chronic hypoxia in the rat
Authors: MacLean M R , Alexander D , Stirrat A , Gallagher M , Douglas S A , Ohlstein E H , Morecroft I , Polland K 
Published: January 2005

Responses to human urotensin‐II (hU‐II) were investigated in human and rat pulmonary arteries. Rat pulmonary arteries: hU‐II was a potent vasoconstrictor of main pulmonary arteries (2–3 mm i.d.) (pEC50, 8.55±0.08, n=21) and was ∼4 fold more potent than endothelin‐1 [ET‐1] (P<0.01), although its Emax was considerably less (∼2.5 fold, P<0.001). The potency of hU‐II increased 2.5 fold with endothelium removal (P<0.05) and after raising vascular tone with ET‐1 (P<0.01). Emax was enhanced ∼1.5 fold in the presence of Nω‐nitro‐L‐arginine methylester (L‐NAME, 100 μM, P<0.01) and ∼2 fold in vessels from pulmonary hypertensive rats exposed to 2 weeks chronic hypoxia (P<0.05). hU‐II did not constrict smaller pulmonary arteries. Human pulmonary arteries (∼250 μm i.d.): in the presence of L‐NAME, 3 out of 10 vessels contracted to hU‐II and this contraction was highly variable. hU‐II is, therefore, a potent vasoconstrictor of rat main pulmonary arteries and this response is increased by endothelial factors, vascular tone and onset of pulmonary hypertension. Inhibition of nitric oxide synthase uncovers contractile responses to hU‐II in human pulmonary arteries.British Journal of Pharmacology (2000) 130, 201–204; doi:10.1038/sj.bjp.0703314
Non‐competitive antagonism of amylin on CGRP1‐receptors in rat coronary small arteries
Authors: Sheykhzade Majid , Nyborg Niels C Berg 
Published: January 2005

We examined the interaction between rat‐amylin and relaxations induced by rat‐αCGRP and isoprenaline in rat isolated coronary small arteries.
Amylin, 0.1–100 nM, had a concentration dependent non‐competitive antagonistic effect on rat‐αCGRP‐induced responses with an EC50 of approximately 1 nM. Amylin did not affect the relaxations induced by isoprenaline at a concentration of 10 nM.
The apparent equilibrium dissociation constant, KA, for CGRP1‐receptors in the rat coronary small arteries was approximately 2 nM. Analysis of the relationship between receptor occupancy and response to rat‐αCGRP indicates that the receptor reserve is small.
Our results show that amylin in low concentrations acts as a selective non‐competitive inhibitor at CGRP1‐receptors in rat isolated coronary small arteries.

British Journal of Pharmacology (2000) 130, 386–390; doi:10.1038/sj.bjp.0703316
Interaction of hypoxanthine/xanthine oxidase with nitrergic relaxation in the porcine gastric fundus
Authors: Colpaert E E , Lefebvre R A 
Published: January 2005

The influence of hypoxanthine (HX)/xanthine oxidase (XO) on short‐term [electrical field stimulation (EFS; 4 Hz) for 10 s and 3 min; bolus of exogenous NO (10−5 M)] and long‐term [EFS (4 Hz) and continuous NO‐infusion for 20 min] nitrergic relaxations was investigated in circular muscle strips of the pig gastric fundus.
HX (3×10−4 M) / XO (64 mu ml−1) did not affect EFS for 10 s and 3 min; the short‐lasting relaxation in response to a bolus of exogenous NO (10−5 M) was changed into a biphasic relaxation with a small and short first phase followed by a larger and prolonged second phase. Cu/Zn superoxide dismutase (Cu/Zn SOD; 1000 u ml−1) and uricase (100 mu ml−1) respectively enhanced the amplitude of the first phase and diminished the amplitude of the second phase. Ascorbate (5×10−4 M) and bilirubin (2×10−4 M) prevented the prolonged component.
Exposure to HX/XO during long‐term EFS elicited a complete, stable reversal of relaxation starting after a delay. During continuous NO‐infusion, HX/XO induced an immediate, complete but transient reversal.
The antioxidants bilirubin, ascorbate, α‐tocopherol, urate, glutathione and Cu/Zn SOD, the hydrogen peroxide degrading enzyme catalase, the hydroxyl radical scavengers dimethylsulphoxide and mannitol, and the cofactor flavin adenine dinucleotide did not influence the reversal induced by HX/XO during either EFS or NO‐infusion. The cell‐permeable manganese SOD mimetic EUK‐8 modified the stable reversal during long‐term EFS into a transient one.
The results suggest that a nitrated uric acid derivative is responsible for the prolonged second phase in the relaxation to a bolus of exogenous NO in the presence of HX/XO. The exact underlying mechanism of the reversal induced by HX/XO during sustained relaxation remains unclear.

British Journal of Pharmacology (2000) 130, 359–366; doi:10.1038/sj.bjp.0703317
Acute blood pressure effects of YC‐1‐induced activation of soluble guanylyl cyclase in normotensive and hypertensive rats
Authors: Rothermund Lars , Friebe Andreas , Paul Martin , Koesling Doris , Kreutz Reinhold 
Published: January 2005

We used YC‐1 as a pharmacological tool to investigate the short‐term blood pressure effects of NO‐independent activation of sGC in normotensive and hypertensive rats. Four groups of normotensive Wistar‐Kyoto rats were treated by i.v. injection with vehicle (V), YC‐1 (YC‐1), sodium nitroprusside (SNP), or YC‐1 and SNP (YC‐1+SNP). Hypertension was induced in four additional groups of WKY rats by 3 weeks of oral treatment with L‐NAME. These animals were investigated with the same protocol as the normotensive animals: L‐NAME/V, L‐NAME/YC‐1, L‐NAME/SNP, L‐NAME/YC‐1+SNP. YC‐1 lowered mean arterial blood pressure (MAP) in normotensive and hypertensive animals similarly to SNP alone (P<0.05, respectively). The combination of YC‐1 with SNP caused a strong decrease of MAP in both the hypertensive and normotensive animals (P<0.05, respectively). SNP with YC‐1 also induced a pronounced cyclic GMP increase in the aorta. This study shows for the first time the blood pressure lowering potential of bimodal targeting of the NO‐sGC‐system.British Journal of Pharmacology (2000) 130, 205–208; doi:10.1038/sj.bjp.0703320
Modulation of 5‐hydroxytryptamine efflux from rat cortical synaptosomes by opioids and nociceptin
Authors: Sbrenna S , Marti M , Morari M , Calo' G , Guerrini R , Beani L , Bianchi C 
Published: January 2005

The modulation of [3H]‐5‐hydroxytryptamine ([3H]‐5‐HT) efflux from superfused rat cortical synaptosomes by delta, kappa, mu and ORL1 opioid receptor agonists and antagonists was studied.
Spontaneous [3H]‐5‐HT efflux was reduced (20% inhibition) by either 0.5 μM tetrodotoxin or Ca2+‐omission. Ten mM K+‐evoked [3H]‐5‐HT overflow was largely Ca2+‐dependent (90%) and tetrodotoxin‐sensitive (50%).
The delta receptor agonist, deltorphin‐I, failed to modulate the K+‐evoked neurotransmitter efflux up to 0.3 μM. The kappa and the mu receptor agonists, U‐50,488 and endomorphin‐1, inhibited K+‐evoked [3H]‐5‐HT overflow (EC50=112 and 7 nM, respectively; Emax=28 and 29% inhibition, respectively) in a norBinaltorphimine‐ (0.3 μM) and naloxone‐ (1 μM) sensitive manner, respectively. None of these agonists significantly affected spontaneous [3H]‐5‐HT efflux.
The ORL1 receptor agonist nociceptin inhibited both spontaneous (EC50=67 nM) and K+‐evoked (EC50=13 nM; Emax=52% inhibition) [3H]‐5‐HT efflux. The effect of NC was insensitive to naloxone (up to 10 μM), but was antagonized by [Nphe1]nociceptin(1‐13)NH2 (a novel selective ORL1 receptor antagonist; pA2=6.7) and by naloxone benzoylhydrazone (pA2=6.3). The ORL1 ligand [Phe1ψ(CH2‐NH)Gly2]nociceptin(1‐13)NH2 also inhibited K+ stimulated [3H]‐5‐HT overflow (EC50=64 nM; Emax=31% inhibition), but its effect was partially antagonized by 10 μM naloxone.
It is concluded that the ORL1 receptor is the most important presynaptic modulator of neocortical 5‐HT release within the opioid receptor family. This suggests that the ORL1/nociceptin system may have a powerful role in the control of cerebral 5‐HT‐mediated biological functions.

British Journal of Pharmacology (2000) 130, 425–433; doi:10.1038/sj.bjp.0703321
A2A adenosine receptor mediated potassium channel activation in rat epididymal smooth muscle
Authors: Haynes John M 
Published: January 2005

The effects of A2 adenosine receptor agonists upon phenylephrine‐stimulated contractility in preparations of rat epididymis were investigated.
Preparations responded to phenylephrine (3 μM) with submaximal contractions. Adenosine and the stable agonists 5′‐N‐ethylcarboxamido‐adenosine (NECA) and 2‐p‐(2‐carboxyethyl) phenethylamino‐N‐ethylcarboxamide adenosine (CGS 21680) inhibited phenylephrine‐induced contractions (potency order, NECA>CGS 21680>adenosine). The A2A receptor‐selective antagonist, 4‐(2‐[7‐amino‐2‐(2‐furyl)[1,2,4]‐triazolo‐[2,3‐a][1,3,5]triazin‐5‐ylamino]ethyl)phenol (ZM 241385, 30 μM) blocked the response to NECA.
The A2A adenosine receptor‐mediated inhibitory responses to NECA were reduced by the KATP channel blocker, glibenclamide (3 μM) and abolished by charybdotoxin (100 nM).
The diterpene forskolin elicited a concentration‐dependent inhibition of phenylephrine (3 μM)‐stimulated contractility (by 62±8% of control at 100 μM). Charybdotoxin (100 nM), but not glibenclamide (3 μM) blocked the forskolin (10 μM) inhibition of phenylephrine‐stimulated contractility.
NECA elicited concentration‐dependent increases in both cyclic AMP and cyclic GMP accumulation which were antagonized by ZM 241385 (30 nM).
The protein kinase G activator, APT‐cyclic GMP (8‐(‐Aminophenylthio) guanosine‐3′,5′‐cyclic monophosphate) and the protein kinase A activator (Sp)‐8‐bromoadenosine‐3′,5′‐cyclic monophosphorothioate (Sp‐8‐Br‐cyclic AMPs), inhibited phenylephrine (3 μM) induced contractions of rat epididymis. Glibenclamide (3 μM), but not charybdotoxin (100 nM), inhibited ATP‐cyclic GMP responses. Charybdotoxin (100 nM), but not glibenclamide (3 μM) reduced the effect of Sp‐8‐Br‐cyclic AMPs.
This study shows that the A2A adenosine receptor inhibition of epididymal contractility may be mediated through the activation of charybdotoxin‐ and glibenclamide‐sensitive potassium channels and may involve the activation of both protein kinases A and G.

British Journal of Pharmacology (2000) 130, 685–691; doi:10.1038/sj.bjp.0703323
Differential effects of UTP and ATP on ion transport in porcine tracheal epithelium
Authors: Inglis S K , Olver R E , Wilson S M 
Published: January 2005

Isolated segments of porcine tracheal epithelium were mounted in Ussing chambers, current required to maintain transepithelial potential difference at 0 mV (short circuit current, ISC) was monitored and effects of nucleotides upon ISC were studied.
Mucosal UTP (100 μM) evoked a transient rise in ISC that was followed by a sustained fall below basal ISC maintained for 30 min. Mucosal ATP (100 μM) also stimulated a transient rise in ISC but in contrast to UTP did not inhibit basal ISC. Submucosal UTP and ATP both transiently increased ISC.
UTP‐prestimulated epithelia were refractory to ATP but prestimulation with ATP did not abolish the response to UTP. The epithelia thus appear to express two populations of apical receptors allowing nucleotides to modulate ISC.
The UTP‐induced rise was reduced by pretreatment with either bumetanide (100 μM), diphenylamin‐2‐carboxylic acid (DPC, 1 mM), or Cl− and HCO3−‐free solution whilst the fall was abolished by amiloride pretreatment.
Thapsigargin (0.3 μM) abolished the UTP‐induced increase in ISC but not the subsequent decrease. Staurosporine (0.1 μM) inhibited basal ISC and blocked UTP‐induced inhibition of ISC. Inhibitors of either protein kinase C (PKC) (D‐erythro sphingosine) or PKA (H89) had no effect.
This study suggests that UTP stimulates Cl− secretion and inhibits basal Na+ absorption. ATP has a similar stimulatory effect, which may be mediated by activation of P2Y2 receptors and an increase in [Ca2+]in, but no inhibitory effect, which is likely mediated by activation of a pyrimidine receptor and possible inhibition of a protein kinase other than PKC or PKA.

British Journal of Pharmacology (2000) 130, 367–374; doi:10.1038/sj.bjp.0703324