Why does every neurotransmission involve the release of ATP?

Terrence Brannon brannon at surf.usc.edu
Fri Jan 16 15:43:14 EST 1998


   Document 5 of 943
AU    FUNK-G-D*;  PARKIS-M-A;  SELVARATNAM-S-R;  WALSH-C
TI    DEVELOPMENTAL MODULATION OF GLUTAMATERGIC INSPIRATORY DRIVE TO 
      HYPOGLOSSAL MOTONEURONS
AD    *UNIV AUCKLAND, DEPT PHYSIOL, FAC MED & HLTH SCI, PRIVATE BAG 92019, 
      AUCKLAND, NEW ZEALAND
CY    NEW ZEALAND
SO    RESPIRATION PHYSIOLOGY, vol. 110, issue 2-3,  (NOV, 1997) : pp. 125-137.
SB    LifeSci
WK    12/21/1997
AB    Proper function of hypoglossal motoneurons (XII MNs) innervating tongue 
      muscles is critical for respiratory control of the airway. 
      Morphological and electrophysiological properties of XII MNs change 
      during postnatal development, as do modulatory systems. Despite these 
      changes, the system producing respiratory movements must remain fully 
      functional throughout life.  Modulatory systems have therefore received 
      considerable attention since coordination of their development with a 
      developing neuromuscular system may be critical for maintenance of 
      continuous, efficient breathing. Developmental modulation of XII 
      inspiratory activity by three transmitter systems is examined.  
      Thyrotropin-releasing hormone (TRH) mediates an increase in MN input 
      resistance (R-N) in juvenile but not neonate MNs, and this likely 
      underlies the developmental increase in TRH potentiation of inspiratory 
      activity.  Norepinephrine (NE) potentiation of inspiratory activity, 
      which in the neonate is produced in part by an alpha(1)-mediated 
      increase in R-N, also increases postnatally. Effects of purinergic 
      transmission on XII inspiratory activity remain constant during the 
      first 2 weeks of postnatal development. Adenosine-triphosphate (ATP) 
      produces tonic excitation and inspiratory potentiation that likely 
      result from activation of postsynaptic P2 receptors.  A secondary 
      inhibitory effect likely results from hydrolysis of ATP to adenosine 
      and activation of presynaptic A1 adenosine receptors.  The functional 
      relevance of these postnatal changes is discussed.  (C) 1997 Elsevier 
      Science B.V.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    42
IN    0034-5687  
SC    WE: RESPIRATORY SYSTEM.  UM: PHYSIOLOGY.
GA    YJ541 (For ordering reprints from ISI)
KW    CONTROL OF BREATHING;  HYPOGLOSSAL MOTONEURONS;  DEVELOPMENT, 
      POSTNATAL;  MEDIATORS, ATP, NOREPINEPHRINE, THYROTROPIN-RELEASING 
      HORMONE;  NERVE, HYPOGLOSSUS
KP    THYROTROPIN-RELEASING-HORMONE;  RAT BRAIN-STEM;  IN-VITRO;  SYNAPTIC 
      TRANSMISSION;  RESPIRATORY RHYTHM;  POSTNATAL CHANGES;  
      RECEPTOR-BINDING;  NEONATAL RAT;  NOREPINEPHRINE;  MECHANISMS

   Document 8 of 943
AU    JEFTINIJA-S-D*;  JEFTINIJA-K-V
TI    ATP STIMULATES RELEASE OF EXCITATORY AMINO-ACIDS FROM CULTURED 
      SCHWANN-CELLS
AD    *IOWA STATE UNIV, DEPT VET ANAT, NEUROSCI PROGRAM, AMES, IA  50011
ZP    50011
CY    USA
SO    NEUROSCIENCE, vol. 82, issue 3,  (FEB, 1998) : pp. 927-934.
SB    LifeSci
WK    12/14/1997
AB    The release of excitatory amino acids from Schwann cell cultures in the 
      rat was monitored using high-performance liquid chromatography.  The 
      basal concentration of glutamate and aspartate was 33 +/- 4 nM (mean 
      +/- S.E.M., n = 12) and 8 +/- 1 nM (mean +/- S.E.M., n = 12), 
      respectively.  ATP (100 mu M) caused a receptor-mediated increase in 
      release of glutamate and aspartate from Schwann cell cultures.  Bath 
      application of adenosine (100 mu M) was without effect on release of 
      excitatory amino acids suggesting involvement of P-2 receptors.  
      Suramin, a competitive antagonist al P-2 receptors, prevented the 
      response to ATP. The release of excitatory amino acids evoked by ATP 
      was not abolished in calcium-depleted saline.  Pretreatment of the 
      Schwann cultures with 50 mu M 
      1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetracetic acid-acetoxymethyl 
      ester (BAPTA-AM) abolished the effect of ATP. ATP-evoked release of 
      glutamate from cultured Schwann cells was significantly reduced by 
      thapsigargin (1 mu M), an inhibitor of Ca2+-ATPase of the Ca2+ pump of 
      internal stores.  U73122, a selective inhibitor of receptor-coupled 
      phospholipase C-dependent processes, abolished stimulatory effect of 
      ATP suggesting that ATP's action is mediated through an inositol 
      1,4,5,-triphosphate-sensitive calcium store.  The action of ATP was not 
      blocked by L-trans-pyrrolidine-2,4-dicarboxylate, an inhibitor of the 
      electrogenic glutamate transporter, nor was it blocked in Na+-free 
      medium, and glutamate release was not stimulated by a depolarizing 
      stimulus, suggesting that ATP-evoked release of glutamate from Schwann 
      cells is not due to the reversal of the glutamate uptake.  An anion 
      transport blocker, furosemide, reduced ATP-induced glutamate release.
      These results suggest that ATP-stimulated glutamate and aspartate 
      release from Schwann cells may be through a calcium-dependent 
      furosemide-sensitive mechanism.  (C) 1997 IBRO.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    50
IN    0306-4522  
SC    RU: NEUROSCIENCES.
GA    YG392 (For ordering reprints from ISI)
KW    ATP;  CALCIUM;  FUROSEMIDE;  GLUTAMATE;  SCHWANN CELLS;  SECRETION
KP    CALCIUM-DEPENDENT RELEASE;  P2Y PURINERGIC RECEPTOR;  SMOOTH-MUSCLE 
      CELLS;  SPINAL DORSAL HORN;  EXTRACELLULAR ATP;  PHOSPHOLIPASE-C;  
      POLYMORPHONUCLEAR NEUTROPHILS;  ADENOSINE 5'-TRIPHOSPHATE;  
      INTRACELLULAR CALCIUM;  SYNAPTIC TRANSMISSION

   Document 21 of 943
AU    DUAN-D-Y*;  YE-L-Y;  YAMAZAKI-J;  HUME-J-R
TI    PURINERGIC ACTIVATION OF A CFTR-LIKE CL- CHANNEL THROUGH 
      PROTEIN-KINASE-C IN MOUSE VENTRICULAR MYOCYTES
AD    UNIV NEVADA, SCH MED, RENO, NV  89557
ZP    89557
CY    USA
SO    CIRCULATION, vol. 96, issue 8, suppl S  (OCT 21, 1997) : pp. 4092-4092.
SB    LifeSci;  ClinMed
WK    11/23/1997
AB    No abstract available.
AA    N
EA    N
LG    eng
PT    MEETING ABSTRACT
IN    0009-7322  
SC    ZD: PERIPHERAL VASCULAR DISEASE.  MA: HEMATOLOGY.
GA    YC880 (For ordering reprints from ISI)

   Document 24 of 943
AU    JONES-S-J*;  GRAY-C;  BOYDE-A;  BURNSTOCK-G
TI    PURINERGIC TRANSMITTERS INHIBIT BONE-FORMATION BY CULTURED OSTEOBLASTS
AD    *UNIV COLL LONDON, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E 6BT, 
      ENGLAND
CY    ENGLAND
SO    BONE, vol. 21, issue 5,  (NOV, 1997) : pp. 393-399.
SB    LifeSci;  ClinMed
WK    11/16/1997
AB    Adenosine triphosphate (ATP) and other purinoceptor agonists cause a 
      transient rise in [Ca2+](i) in cultured osteoblast-like cells and have 
      a mitogenic effect, as does parathyroid hormone (PTH), and there is 
      evidence that ATP and PTH can act synergistically on osteoblasts.  The 
      likelihood that nucleotides, acting through purinoceptors, are 
      important local factors in bone remodeling is therefore considerable.  
      However, their effect on bone formation is unknown.  We recently 
      developed a culture system in which appositional bone formation occurs 
      only in narrow grooves cut in a substratum.  We have used this as an 
      assay to measure the effects of ATP (50 and 500 mu mol/L), ATP gamma S 
      (20 mu mol/L), 2-MeSATP (2 and 20 mu mol/L), uridine triphosphate (UTP) 
      (0.2, 2, and 20 mu mol/L), adenosine (20 mu mol/L), bovine PTH (0.25 
      and 0.5 IU/mL), rat PTH1-34 (10(-8) and 10(-7) mol/L), and rat 
      PTHrP1-40 (10(-9) and 10(-8) mol/L) on bone formation by rat calvarial 
      osteoblasts. The culture medium was renewed 3 times/week (every 2 or 3 
      days), and the number of bone loci and length and area of Alizarin 
      red-stained mineralized bone formed in the grooves of each specimen in 
      16-29 days were measured.  Compared with controls, ATP gamma S, 
      2-MeSATP, and ATP reduced the amount of bone formed in a 2-3 week 
      culture period.  Adenosine had no effect, and UTP either had no effect 
      or at 2 mu mol/L stimulated bone formation.  PTH and PTHrP completely 
      abolished bone formation in 4 week cultures.  Our findings are 
      consistent with evidence for more than one P2 purinoceptor subtype in 
      bone, and show for the first time that the effect of ATP on 
      appositional bone formation by osteoblasts in vitro is, like PTH and 
      PTHrP, inhibitory.  (C) 1997 by Elsevier Science Inc.  All rights 
      reserved.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    40
IN    8756-3282  
SC    IA: ENDOCRINOLOGY AND METABOLISM.
GA    YD853 (For ordering reprints from ISI)
KW    OSTEOBLASTS;  BONE FORMATION;  ADENOSINE TRIPHOSPHATE;  PURINOCEPTORS;  
      PARATHYROID HORMONE;  PARATHYROID HORMONE RELATED PROTEIN
KP    PARATHYROID-HORMONE;  IN-VITRO;  INTRACELLULAR CALCIUM;  SIGNALING 
      PATHWAYS;  CELLS;  ATP;  MINERALIZATION;  PURINOCEPTORS;  CHONDROCYTES; 
      OSTEOCLASTS

   Document 26 of 943
AU    COOK-S-P*;  MCCLESKEY-E-W
TI    DESENSITIZATION, RECOVERY AND CA2+-DEPENDENT MODULATION OF ATP-GATED 
      P2X RECEPTORS IN NOCICEPTORS
AD    *OREGON HLTH SCI UNIV, VOLLUM INST, L474, PORTLAND, OR  97201
ZP    97201
CY    USA
SO    NEUROPHARMACOLOGY, vol. 36, issue 9,  (SEP, 1997) : pp. 1303-1308.
SB    LifeSci
WK    11/16/1997
AB    We have shown the presence and activity of ATP-gated ion channels (P2X 
      receptors) in nociceptive nerve endings, supporting the theory that 
      these channels mediate some forms of nociception [Cook S. P., 
      Vulchanova L., Hargreaves K. M., Elde R. and McCleskey E. W. (1997) 
      Distinct ATP receptors on pain-sensing and stretch-sensing neurons.  
      Nature 387, 505-508]. The kinetics and pharmacology of ATP-gated 
      currents in nociceptors suggest that the channels are comprised of 
      either homomeric or heteromeric combinations of P2X3 receptors.  
      Consistent with the diverse nature of P2X structure, 
      electrophysiological responses of rat tooth-pulp nociceptors fall into 
      two distinct classes based on desensitization and recovery kinetics.  
      Here, we quantified the dramatic differences in desensitization 
      kinetics of transient and persistent currents.  The major component of 
      transient P2X current desensitized with a tau(decay) = 32 +/- 2 msec, 
      while persistent current desensitized >100-fold more slowly, tau(decay) 
      = 4000 +/- 320 msec, Both currents recovered from desensitization in 
      minutes: tau(recovery) = 4 min for transient current, and tau(decay) = 
      0.7 +/- 0.2 min for persistent current.  Persistent current recovery 
      was often accompanied by a current ''overrecovery'' that averaged ca 
      threefold magnitude prior to desensitization.  Comparison of ATP 
      current in elevated Ca-ext(2+) also revealed differences in transient 
      and persistent currents.  In 2 mM Ca-ext(2+) medium, decrease of 
      Na-ext(+) resulted in an almost complete reduction of persistent, but 
      not transient, current.  Subsequent elevation of Ca-ext(2+) greatly 
      increased the transient, but not persistent, current.  Mechanistic 
      explanations for either the increase in transient current magnitude by 
      elevated Ca-ext(2+), or persistent current overrecovery may reflect 
      endogenous pathways for P2X receptor modulation.  (C) 1997 Elsevier 
      Science Ltd.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    25
IN    0028-3908  
SC    TU: PHARMACOLOGY AND PHARMACY.  RU: NEUROSCIENCES.
GA    YD892 (For ordering reprints from ISI)
KW    SENSORY NEURONS;  P2X RECEPTOR;  DESENSITIZATION;  PURINERGIC;  
      NOCICEPTOR
KP    RAT SENSORY NEURONS;  ION CHANNELS;  EXTRACELLULAR ATP;  ZN2+;  
      RESPONSES;  CURRENTS;  CELLS

   Document 28 of 943
AU    COLLO-G;  NEIDHART-S;  KAWASHIMA-E;  KOSCOVILBOIS-M;  NORTH-R-A;  
      BUELL-G*
TI    TISSUE DISTRIBUTION OF THE P2X(7) RECEPTOR
AD    *GLAXO WELLCOME RES & DEV LTD, GENEVA BIOMED RES INST, PLAN LES OUATES, 
      CH-1228 GENEVA, SWITZERLAND
      GLAXO WELLCOME RES & DEV LTD, GENEVA BIOMED RES INST, CH-1228 GENEVA, 
      SWITZERLAND
CY    SWITZERLAND
SO    NEUROPHARMACOLOGY, vol. 36, issue 9,  (SEP, 1997) : pp. 1277-1283.
SB    LifeSci
WK    11/16/1997
AB    The P2X(7) receptor is a bifunctional molecule.  The binding of ATP 
      induces within milliseconds the opening of a channel selective for 
      small cations, and within seconds a larger pore opens which allows 
      permeation by molecules as large as propidium dyes (629 Da). In situ 
      hybridization using a digoxigenin-labelled riboprobe, and 
      immunohistochemistry using an antibody raised against a C-terminal 
      peptide sequence, were used to determine the distribution of the P2X(7) 
      receptor mRNA and protein in rat and mouse tissues and cell lines.  The 
      brain of newborn rats showed a 6 kb RNA by Northern blotting, but this 
      was not detectable in adult brain.  By in situ hybridization and 
      immunohistochemistry, there was heavy labelling of ependymal cells in 
      both newborn and adult brain, but the brain parenchyma showed no 
      labelling. However, P2X(7) receptor-immunoreactive cells appeared in 
      the penumbral region around an area of necrosis evoked by prior 
      occlusion of the middle cerebral artery, suggesting expression of the 
      receptor by activated microglia.  NTW8 cells, a mouse microglial cell 
      Line, strongly expressed the P2X(7) receptor mRNA and protein.  The 
      P2X(7) receptor mRNA and protein were also observed in the majority of 
      bone marrow cells, including those separately identified by their 
      expression of other antigens as granulocytes, monocyte/macrophages and 
      B lymphocytes.  The expression of P2X(7) receptor by brain macrophages 
      rather than neurons would be consistent with a role in brain repair 
      following inflammation, infarction or immune insult.  (C) 1997 Elsevier 
      Science Ltd.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    33
IN    0028-3908  
SC    TU: PHARMACOLOGY AND PHARMACY.  RU: NEUROSCIENCES.
GA    YD892 (For ordering reprints from ISI)
KW    IN SITU HYBRIDIZATION;  IMMUNOHISTOCHEMISTRY;  P2X(7) RECEPTOR;  
      MACROPHAGE;  MONOCYTE;  MICROGLIA;  PURINERGIC RECEPTORS;  ATP
KP    GATED ION CHANNELS;  EXTRACELLULAR ATP;  P-2X RECEPTOR;  MICROGLIAL 
      CELLS;  PLASMA-MEMBRANE;  MOUSE-BRAIN;  PURINOCEPTORS;  RAT;  RELEASE

   Document 47 of 943
AU    NIEBER-K;  POELCHEN-W;  ILLES-P*
TI    ROLE OF ATP IN FAST EXCITATORY SYNAPTIC POTENTIALS IN LOCUS-COERULEUS 
      NEURONS OF THE RAT
AD    *UNIV LEIPZIG, INST PHARMAKOL & TOXIKOL, D-04107 LEIPZIG, GERMANY
      UNIV LEIPZIG, INST PHARMAKOL & TOXIKOL, D-04107 LEIPZIG, GERMANY
      UNIV LEIPZIG, INST PHARM, ABT PHARMAKOL NAT WISSENSCH, D-04103 LEIPZIG, 
      GERMANY
CY    GERMANY
SO    BRITISH JOURNAL OF PHARMACOLOGY, vol. 122, issue 3,  (OCT, 1997) : pp. 
      423-430.
SB    LifeSci
WK    10/19/1997
AB    1.  Intracellular recordings were made in a pontine slice preparation 
      of the rat brain containing the nucleus locus coeruleus (LC). The 
      pressure application of alpha,beta-methylene ATP (alpha,beta-meATP) 
      caused reproducible depolarizations which were depressed by suramin (30 
      mu M) and abolished by suramin (100 mu M). 
      Pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 10, 30 
      mu M) also concentration-dependently inhibited the 
      alpha,beta-meATP-induced depolarization, although with a much slower 
      timecourse than suramin.  Almost complete inhibition developed with 30 
      mu M PPADS. Reactive blue 2 (30 mu M) did not alter the effect of 
      alpha,beta-meATP, while reactive blue 2 (100 mu M) slightly depressed 
      it.
      2.  Pressure-applied 
      (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) 
      also depolarized LC neurones.  Kynurenic acid (500 mu M) depressed and 
      6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 50 mu M) abolished the 
      response to AMPA. Suramin (100 mu M) potentiated the AMPA effect.
      3.  Pressure-applied noradrenaline hyperpolarized LC neurones. Suramin 
      (100 mu M) did not after the effect of noradrenaline.
      4.  Focal electrical stimulation evoked biphasic synaptic potentials 
      consisting of a fast depolarization (p.s.p.)  followed by a slow 
      hyperpolarization (i.p.s.p.). A mixture of 
      D(-)-2-amino-5-phosphonopentanoic acid (AP-5; 50 mu M), CNQX (50 mu M) 
      and picrotoxin (100 mu M) depressed both the p.s.p.  and the i.p.s.p.  
      Under these conditions suramin (100 mu M) markedly inhibited the 
      p.s.p., but did not alter the i.p.s.p.  In the combined presence of 
      AP-5 (50 mu M), CNQX (50 mu M), picrotoxin (100 mu M), strychnine (0.1 
      mu M), tropisetron (0.5 mu M) and hexamethonium (100 mu M), a high 
      concentration of suramin (300 mu M) almost abolished the p.s.p.  
      without changing the i.p.s.p.
      5.  In the presence of kynurenic acid (500 mu M) and picrotoxin (100 mu 
      M), PPADS (30 mu M) depressed the p.s.p.  Moreover, the application of 
      suramin (100 mu M) to the PPADS (30 mu M)-containing medium failed to 
      cause any further inhibition. Neither PPADS (30 mu M) nor suramin (100 
      mu M) altered the i.p.s.p.
      6.  It was concluded that the cell somata of LC. neurones are endowed 
      with excitatory P2-purinoceptors.  ATP may be released either as the 
      sole transmitter from purinergic neurones terminating at the LC or as a 
      co-transmitter of noradrenaline from recurrent axon collaterals or 
      dendrites of the LC neurones themselves.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    47
IN    0007-1188  
SC    TU: PHARMACOLOGY AND PHARMACY.  CQ: BIOCHEMISTRY AND MOLECULAR BIOLOGY.
GA    XZ409 (For ordering reprints from ISI)
KW    ATP;  NORADRENALINE;  LOCUS COERULEUS
KP    GATED ION CHANNELS;  NERVOUS-SYSTEM;  CERULEUS NEURONS;  
      P-2-PURINOCEPTOR ANTAGONISTS;  ADENOSINE 5'-TRIPHOSPHATE;  P-2X 
      PURINOCEPTORS;  GUINEA-PIG;  IN-VITRO;  RECEPTOR;  INHIBITION

   Document 61 of 943
AU    BARDONI-R*;  GOLDSTEIN-P-A;  LEE-C-J;  GU-J-G;  MACDERMOTT-A-B
TI    ATP P-2X RECEPTORS MEDIATE FAST SYNAPTIC TRANSMISSION IN THE DORSAL 
      HORN OF THE RAT SPINAL-CORD
AD    *UNIV MODENA, SEZ FISIOL, DIPARTIMENTO SCI BIOMED, VIA CAMPI 287, 
      I-41100 MODENA, ITALY
      COLUMBIA UNIV, DEPT PHYSIOL & CELLULAR BIOPHYS, NEW YORK, NY 10032
      COLUMBIA UNIV, DEPT ANESTHESIOL, NEW YORK, NY  10032
      COLUMBIA UNIV, CTR NEUROBIOL & BEHAV, NEW YORK, NY  10032
ZP    10032
CY    ITALY
      USA
SO    JOURNAL OF NEUROSCIENCE, vol. 17, issue 14,  (JUL 15, 1997) : pp. 
      5297-5304.
SB    LifeSci
WK    09/21/1997
AB    ATP has been proposed to mediate synaptic transmission in the spinal 
      card dorsal horn, particularly in the pathway carrying nociceptive 
      information.  Using transverse spinal cord slices from postnatal rats, 
      we show that EPSCs mediated by P-2x receptors, and presumably activated 
      by synaptically released ATP, are evoked in a subpopulation of spinal 
      cord lamina II neurons, a region known to receive strong input from 
      nociceptive primary afferents.  The P-2x receptors on acutely 
      dissociated dorsal horn neurons are nondesensitizing, insensitive to 
      alpha beta methylene ATP, and show strong but variable sensitivity to 
      the antagonists suramin and 
      pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS). These 
      characteristics are consistent with a heterogeneous population of P-2x 
      receptors, the composition of which includes P-2x2 P-2x4 and P-2x6 
      receptor subtypes.  Our results suggest that ATP-activated P-2x 
      receptors in lamina II of the rat spinal cord may play a role in 
      transmitting or modulating nociceptive information.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    36
IN    0270-6474  
SC    RU: NEUROSCIENCES.
GA    XV075 (For ordering reprints from ISI)
KW    ATP;  PURINERGIC RECEPTORS;  SYNAPTIC TRANSMISSION;  SPINAL CORD;  RAT; 
      PATCH-CLAMP TECHNIQUE;  SLICE PREPARATION
KP    GATED ION CHANNELS;  INTRACELLULAR CALCIUM;  EXTRACELLULAR ATP;  
      SENSORY NEURONS;  FAST KINETICS;  CURRENTS;  BRAIN;  NMDA;  CELLS

   Document 68 of 943
AU    CHO-H;  HARADA-N*;  YAMASHITA-T
TI    EXTRACELLULAR ATP-INDUCED CA2+ MOBILIZATION OF TYPE-I SPIRAL 
      GANGLION-CELLS FROM THE GUINEA-PIG COCHLEA
AD    *KANSAI MED UNIV, DEPT OTOLARYNGOL, MORIGUCHI, OSAKA 570, JAPAN
      KANSAI MED UNIV, DEPT OTOLARYNGOL, MORIGUCHI, OSAKA 570, JAPAN
CY    JAPAN
SO    ACTA OTO-LARYNGOLOGICA, vol. 117, issue 4,  (JUL, 1997) : pp. 545-552.
SB    LifeSci;  ClinMed
WK    09/07/1997
AB    Intracellular calcium concentrations ([Ca2+](i)) in type I cochlear 
      spiral ganglion cells (SGCs) of the guinea pig were measured by digital 
      imaging microscopy and the Ca2+-sensitive dye Fura-2.  Extracellular 
      ATP induced elevation of [Ca2+](i) in type T SGCs in a 
      concentration-dependent manner.  The ATP-induced elevation of [Ca2+](i) 
      in SGC was even evident in the Ca2+-free solution, thereby suggesting 
      that ATP induces a Ca2+-release from intracellular stores in SGCs.  
      Suramin and reactive blue 2, both antagonists for the P-2-purinergic 
      receptor, inhibited the [Ca2+](i) increase in SGCs induced by 
      extracellular ATP in a dose-dependent manner.  Adenosine did not induce 
      any changes of [Ca2+](i) in SGC. These results suggest that type I SGCs 
      may possess P-2-purinergic receptor but not P-1-purinergic receptor. 
      Extracellular ATP induced a [Ca2+](i) increase in type I SGCs, with and 
      without neuritic processes, while L-glutamate increased [Ca2+](i) in 
      type I SGCs with neuritic processes, but not SGCs without neuritic 
      processes.  The ATP-induced [Ca2+](i) increase was almost equal in both 
      soma and processes.  Therefore, the distribution of P-2-purinergic 
      receptor in type I SGCs may be homogeneous in soma and processes.  
      Based on these observations, we suggest that extracellular ATP may act 
      as a neurotransmitter or neuromodulator of the hair cell-afferent nerve 
      synapse in the guinea pig cochlea.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    25
IN    0001-6489  
SC    TD: OTORHINOLARYNGOLOGY.
GA    XR784 (For ordering reprints from ISI)
KW    AFFERENT NEUROTRANSMITTER;  ATP;  COCHLEA;  FURA-2;  P-2-PURINERGIC 
      RECEPTOR;  SPIRAL GANGLION CELLS
KP    HAIR-CELLS;  NEUROTRANSMITTERS;  RESPONSES;  CURRENTS;  CALCIUM

   Document 175 of 943
AU    HARTLEY-S-A;  KOZLOWSKI-R-Z*
TI    ELECTROPHYSIOLOGICAL CONSEQUENCES OF PURINERGIC RECEPTOR STIMULATION IN 
      ISOLATED RAT PULMONARY ARTERIAL MYOCYTES
AD    *UNIV OXFORD, DEPT PHARMACOL, MANSFIELD RD, OXFORD OX1 3QT, ENGLAND
      UNIV OXFORD, DEPT PHARMACOL, OXFORD OX1 3QT, ENGLAND
CY    ENGLAND
SO    CIRCULATION RESEARCH, vol. 80, issue 2,  (FEB, 1997) : pp. 170-178.
SB    LifeSci
WK    02/16/1997
AB    Neither the electrophysiological effects of purinergic receptor 
      stimulation nor the role of ATP in regulating the tone of pulmonary 
      arterial smooth muscle has been determined.  Therefore, we investigated 
      the effects of purine nucleotides on acutely dissociated smooth muscle 
      cells from rat small pulmonary arteries using the patch-clamp recording 
      technique.  Extracellular application of ATP activated a fast transient 
      inward current (which decayed in the continued presence of the 
      nucleotide) and produced sustained periodic oscillations of 
      predominantly inward current.  Pharmacological and anion substitution 
      experiments revealed that the transient inward current was carried by 
      the movement of cations.  In contrast, the peri odic oscillations of 
      current were due primarily to a Ca2+-activated Cl- current (I-Cl,I-Ca) 
      dependent on the release of Ca2+ from intracellular stores.  
      Experiments using ATP analogues revealed the following order of potency 
      for activation of the fast transient inward current: 2-methylthio ATP 
      (2-meSATP)>ATP>alpha,beta-methylene ATP (alpha,beta-meATP)much greater 
      than ADP>UTP=adenosine.  Cross desensitization was seen between 
      applications of ATP, alpha,beta-meATP, and 2-meSATP, suggesting that 
      these agonists act via a common site.  The order of potency for 
      activation of I-Ca,I-Cl was UTP=ATP much greater than ADP greater than 
      or equal to 2-meSATP>alpha,beta-meATP=adenosine.  Both the fast 
      transient inward current and I-Cl,I-Ca evoked by ATP and its analogues 
      were abolished by the nonselective P-2 purinoceptor antagonist suramin. 
      These results show the existence of P-2X and P-2U purinoceptor subtypes 
      in pulmonary arterial smooth muscle cells.  Stimulation of these 
      receptors results in activation of a fast transient inward cation 
      current and I-Cl,I-Ca, respectively.  It is likely that ATP acts via 
      these receptor subtypes to regulate pulmonary arterial tone under 
      physiological or pathological conditions.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    54
IN    0009-7330  
SC    MA: HEMATOLOGY.  ZD: PERIPHERAL VASCULAR DISEASE.
GA    WE959 (For ordering reprints from ISI)
KW    PULMONARY ARTERY;  P-2 PURINOCEPTOR;  PURINE NUCLEOTIDE;  CL- CHANNEL
KP    SMOOTH-MUSCLE CELLS;  RABBIT PORTAL-VEIN;  ADENOSINE-TRIPHOSPHATE;  EAR 
      ARTERY;  P2-PURINOCEPTOR SUBTYPES;  P2-PURINERGIC RECEPTORS;  
      EXTRACELLULAR ATP;  ENDOTHELIAL-CELLS;  SENSORY NEURONS;  ION CHANNELS

   Document 183 of 943
AU    HALLIDAY-F-C*;  GIBB-A-J
TI    NEUROPHARMACOLOGY - A PART FOR PURINES IN PATTERN GENERATION
AD    *UNIV COLL LONDON, DEPT PHARMACOL, GOWER ST, LONDON WC1E 6BT, ENGLAND
CY    ENGLAND
SO    CURRENT BIOLOGY, vol. 7, issue 1,  (JAN 1, 1997) : pp. R47-R49.
SB    LifeSci
WK    02/09/1997
AB    Purinergic transmission has been found to play a key role in the neural 
      control of rhythmic swimming behaviour in Xenopus embryos; it may have 
      similar importance in other vertebrate motor behaviours.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    12
IN    0960-9822  
SC    CQ: BIOCHEMISTRY AND MOLECULAR BIOLOGY.  CU: BIOLOGY.
GA    WE221 (For ordering reprints from ISI)
KP    EXPRESSION;  RECEPTOR

   Document 24 of 943
AU    JONES-S-J*;  GRAY-C;  BOYDE-A;  BURNSTOCK-G
TI    PURINERGIC TRANSMITTERS INHIBIT BONE-FORMATION BY CULTURED OSTEOBLASTS
AD    *UNIV COLL LONDON, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E 6BT, 
      ENGLAND
CY    ENGLAND
SO    BONE, vol. 21, issue 5,  (NOV, 1997) : pp. 393-399.
SB    LifeSci;  ClinMed
WK    11/16/1997
AB    Adenosine triphosphate (ATP) and other purinoceptor agonists cause a 
      transient rise in [Ca2+](i) in cultured osteoblast-like cells and have 
      a mitogenic effect, as does parathyroid hormone (PTH), and there is 
      evidence that ATP and PTH can act synergistically on osteoblasts.  The 
      likelihood that nucleotides, acting through purinoceptors, are 
      important local factors in bone remodeling is therefore considerable.  
      However, their effect on bone formation is unknown.  We recently 
      developed a culture system in which appositional bone formation occurs 
      only in narrow grooves cut in a substratum.  We have used this as an 
      assay to measure the effects of ATP (50 and 500 mu mol/L), ATP gamma S 
      (20 mu mol/L), 2-MeSATP (2 and 20 mu mol/L), uridine triphosphate (UTP) 
      (0.2, 2, and 20 mu mol/L), adenosine (20 mu mol/L), bovine PTH (0.25 
      and 0.5 IU/mL), rat PTH1-34 (10(-8) and 10(-7) mol/L), and rat 
      PTHrP1-40 (10(-9) and 10(-8) mol/L) on bone formation by rat calvarial 
      osteoblasts. The culture medium was renewed 3 times/week (every 2 or 3 
      days), and the number of bone loci and length and area of Alizarin 
      red-stained mineralized bone formed in the grooves of each specimen in 
      16-29 days were measured.  Compared with controls, ATP gamma S, 
      2-MeSATP, and ATP reduced the amount of bone formed in a 2-3 week 
      culture period.  Adenosine had no effect, and UTP either had no effect 
      or at 2 mu mol/L stimulated bone formation.  PTH and PTHrP completely 
      abolished bone formation in 4 week cultures.  Our findings are 
      consistent with evidence for more than one P2 purinoceptor subtype in 
      bone, and show for the first time that the effect of ATP on 
      appositional bone formation by osteoblasts in vitro is, like PTH and 
      PTHrP, inhibitory.  (C) 1997 by Elsevier Science Inc.  All rights 
      reserved.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    40
IN    8756-3282  
SC    IA: ENDOCRINOLOGY AND METABOLISM.
GA    YD853 (For ordering reprints from ISI)
KW    OSTEOBLASTS;  BONE FORMATION;  ADENOSINE TRIPHOSPHATE;  PURINOCEPTORS;  
      PARATHYROID HORMONE;  PARATHYROID HORMONE RELATED PROTEIN
KP    PARATHYROID-HORMONE;  IN-VITRO;  INTRACELLULAR CALCIUM;  SIGNALING 
      PATHWAYS;  CELLS;  ATP;  MINERALIZATION;  PURINOCEPTORS;  CHONDROCYTES; 
      OSTEOCLASTS

   Document 20 of 85
AU    THORNE-P-R*;  HOUSLEY-G-D
TI    PURINERGIC SIGNALING IN SENSORY SYSTEMS
AD    *UNIV AUCKLAND, DEPT PHYSIOL, PRIVATE BAG 92019, AUCKLAND, NEW ZEALAND
CY    NEW ZEALAND
SO    SEMINARS IN THE NEUROSCIENCES, vol. 8, issue 4,  (AUG, 1996) : pp. 
      233-246.
SB    LifeSci
WK    08/18/1996
AB    Extracellular purines play multiple roles in a variety of sensory 
      systems acting as neural signalling and humoral factors via 
      purinoceptors.  For example, ATP and adenosine have a neurosignalling 
      role in autonomic sensory-motor reflexes, mechanoreception and 
      chemoreception mediated via vagus nerve afferents, and in, nociception. 
      Purinergic neuromodulation of vision via adenosine in the retina is 
      well established and there is mounting evidence for a neuromodulatory 
      role for ATP in the inner ear.  Humoral purinergic actions are found in 
      the eye where adenosine clearly has an important vascular and humoral 
      influence and in the inner ear where ATP probably regulates fluid 
      homeostasis, hearing sensitivity and development.  Clearly purinergic 
      signalling underpins the physiology of many of the body's sensory 
      systems.  (C) 1996 Academic Press Ltd
AA    N
EA    Y
LG    eng
PT    REVIEW
RF    143
IN    1044-5765  
SC    RU: NEUROSCIENCES.
GA    VA666 (For ordering reprints from ISI)
KW    EYE;  HEARING;  INNER EAR;  NOCICEPTION;  OLFACTION
KP    GUINEA-PIG COCHLEA;  OUTER HAIR-CELLS;  CHICK-EMBRYO RETINA;  
      NONADRENERGIC NONCHOLINERGIC NEUROTRANSMISSION;  ADENOSINE 
      5'-TRIPHOSPHATE ATP;  OLFACTORY RECEPTOR NEURONS;  H-3 NORADRENALINE 
      RELEASE;  CILIARY EPITHELIAL-CELLS;  ISOLATED VAGUS NERVE;  DORSAL HORN 
      NEURONS

   Document 29 of 85
AU    BURNSTOCK-G*
TI    NORADRENALINE AND ATP - COTRANSMITTERS AND NEUROMODULATORS
AD    *UNIV LONDON UNIV COLL, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E 
      6BT, ENGLAND
      UNIV COLL LONDON, CTR NEUROSCI, LONDON, ENGLAND
CY    ENGLAND
SO    JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, vol. 46, issue 4,  (DEC, 1995) 
      : pp. 365-384.
SB    LifeSci
WK    01/14/1996
AB    Adenosine 5'-triphosphate (ATP) is a cotransmitter with noradrenaline 
      (NA) in sympathetic nerves supplying the vas deferens and a number of 
      blood vessels.  ATP is responsible for the excitatory junctional 
      potentials (EJPs) in response to single nerve impulses and the initial 
      twitch responses of the smooth muscle, while NA produces the 
      longer-lasting tonic contractions. The proportions of ATP to NA vary 
      between different sympathetic nerves; they also change during 
      development and in some pathological conditions, including 
      hypertension.  Prejunctional neuromodulation of release of the two 
      cotransmitters appears to involve independent mechanisms and is 
      frequency dependent; this raises the question of whether ATP and NA are 
      stored in separate vesicles or whether there are subpopulations of 
      sympathetic nerves with a predominance of ATP or NA. ATP and NA have 
      synergistic postjunctional actions, whether excitatory (as in the vas 
      deferens and most blood vessels) or inhibitory (as in rabbit coronary 
      vessels). It is suggested that use of the term 'adrenergic nerves' as a 
      synonym for sympathetic nerves is no longer appropriate, although 
      'adrenergic transmission' or 'purinergic transmission' are still useful 
      terms.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    195
IN    0867-5910  
SC    UM: PHYSIOLOGY.
GA    TM027 (For ordering reprints from ISI)
KW    PURINERGIC;  SYMPATHETIC;  HYPERTENSION;  PLASTICITY;  NEUROPEPTIDES;  
      NEUROTRANSMISSION
KP    PIG VAS-DEFERENS;  SYMPATHETIC-NERVE STIMULATION;  RABBIT EAR ARTERY;  
      DOG MESENTERIC-ARTERY;  SMOOTH-MUSCLE CELLS;  VASCULAR 
      ADRENERGIC-NERVES;  BETA-METHYLENE ATP;  RAT CAUDAL ARTERY;  
      GUINEA-PIG;  ADENOSINE-TRIPHOSPHATE

   Document 66 of 85
AU    BURNSTOCK-G*
TI    PHYSIOLOGICAL AND PATHOLOGICAL ROLES OF PURINES - AN UPDATE
AD    *UNIV LONDON UNIV COLL, DEPT ANAT & DEV BIOL, GOWER ST, LONDON WC1E 
      6BT, ENGLAND
      UNIV LONDON UNIV COLL, CTR NEUROSCI, LONDON WC1E 6BT, ENGLAND
CY    ENGLAND
SO    DRUG DEVELOPMENT RESEARCH, vol. 28, issue 3,  (MAR, 1993) : pp. 195-206.
SB    LifeSci
WK    04/11/1993
AB    In this review article, the early history of studies of purinergic 
      neurotransmission and of purinoceptor subclassification is described.  
      This is followed by a survey of current knowledge of the distribution 
      of purinoceptors and of the physiological roles of purines in the 
      nervous system, muscle, secretory, endocrine and immune cells, as well 
      as in spermatocytes, osteoblasts, fibroblasts, and tumour cells.  
      Recent studies of transduction mechanisms for different purinoceptor 
      subtypes, as well as reports of the molecular properties of encoding 
      genes for purinoceptors, are reviewed.  The evolution of purinergic 
      mechanisms and the long-term 'trophic' actions of purines are 
      discussed.  Finally, the clinical potential of purines and related 
      compounds for various cardiovascular and behavioural disorders, as well 
      as for inflammation and cancer are considered.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    216
IN    0272-4391  
SC    TU: PHARMACOLOGY AND PHARMACY.
GA    KV613 (For ordering reprints from ISI)
KP    A1 ADENOSINE RECEPTOR;  PIG VAS-DEFERENS;  VASCULAR ENDOTHELIAL-CELLS;  
      CEREBRAL CORTICAL-NEURONS;  BRAIN MESSENGER-RNA;  OUTER HAIR-CELLS;  
      PROTEIN KINASE-C;  EXTRACELLULAR ATP;  GUINEA-PIG;  SENSORY NEURONS

   Document 81 of 85
AU    CRAIG-C-G*;  WHITE-T-D
TI    LOW-LEVEL N-METHYL-D-ASPARTATE RECEPTOR ACTIVATION PROVIDES A 
      PURINERGIC INHIBITORY THRESHOLD AGAINST FURTHER 
      N-METHYL-D-ASPARTATE-MEDIATED NEUROTRANSMISSION IN THE CORTEX
AD    *DALHOUSIE UNIV, DEPT PHARMACOL, HALIFAX B3H 4H7, NS, CANADA
CY    CANADA
SO    JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, vol. 260, issue 
      3,  (MAR, 1992) : pp. 1278-1284.
SB    LifeSci
WK    01/01/1992
AB    N-methyl-D-aspartate (NMDA) is 33 times more potent at releasing 
      adenosine than it is at releasing [H-3]norepinephrine from slices of 
      rat parietal cortex.  Consequently, maximal adenosine release occurs at 
      levels of NMDA receptor activation which release little norepinephrine. 
      The potential modulatory role of the adenosine released during NMDA 
      receptor activation on NMDA-evoked [H-3]norepinephrine release was 
      investigated.  The A1-selective agonist 
      R-(-)N6-(2-phenylisopropyl)adenosine (10-mu-M) decreased 100-mu-M 
      NMDA-evoked [H-3]norepinephrine release by 27%; this was reversed by 
      the P1 antagonist 8-phenyltheophylline (8-PT, 10-mu-M), indicating that 
      NMDA-evoked norepinephrine release from cortical slices is susceptible 
      to purinergic modulation.  On the other hand, 8-PT had no effect on 
      [H-3]norepinephrine release evoked by 100-mu-M NMDA, suggesting that 
      endogenous adenosine, released during NMDA receptor activation, does 
      not modulate [H-3]norepinephrine release.  However, [H-3]norepinephrine 
      release precedes adenosine release, so that the released adenosine may 
      not be temporally available to modulate [H-3]norepinephrine release. 
      Pretreatment with a concentration of NMDA (10-mu-M) which releases 
      substantial endogenous adenosine, but very little [H-3]norepinephrine 
      decreased subsequent 100-mu-M NMDA-evoked [H-3]norepinephrine release 
      by 52%. 8-PT partially reversed this inhibition, indicating that 
      prereleased adenosine, acting at P1 purinoceptors, modulated subsequent 
      NMDA-evoked [H-3]norepinephrine release.  These results suggest that 
      adenosine, released during submaximal NMDA receptor activation, may 
      provide an inhibitory threshold which must be overcome in order for 
      other NMDA-mediated processes to proceed maximally.
AA    N
EA    Y
LG    eng
PT    ARTICLE
RF    60
IN    0022-3565  
SC    TU: PHARMACOLOGY AND PHARMACY.
GA    HJ019 (For ordering reprints from ISI)
KP    LONG-TERM POTENTIATION;  CENTRAL NERVOUS-SYSTEM;  RAT HIPPOCAMPAL 
      SLICES;  EXCITATORY AMINO-ACIDS;  EVOKED RELEASE;  EPILEPTIFORM 
      ACTIVITY;  ENDOGENOUS ADENOSINE;  NMDA RECEPTORS;  GLUTAMATE RELEASE;  
      AMINOBUTYRIC-ACID


CP    Copyright US/Pacific, Current Contents(tm) from ISI, all rights reserved.

   Document 199 of 943
AU    BRAKE-A-J*;  JULIUS-D
TI    SIGNALING BY EXTRACELLULAR NUCLEOTIDES
AD    *UNIV CALIF SAN FRANCISCO, DEPT MOL & CELLULAR PHARMACOL, CELL BIOL 
      PROGRAM, SAN FRANCISCO, CA  94143
      UNIV CALIF SAN FRANCISCO, DEPT MOL & CELLULAR PHARMACOL, PROGRAM 
      NEUROSCI, SAN FRANCISCO, CA  94143
ZP    94143
CY    USA
SO    ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, vol. 12,  (1996) : pp. 
      519-541.
SB    LifeSci
WK    01/12/1997
AB    ATP and other nucleotides can be released from cells through regulated 
      pathways, or following the loss of plasma membrane integrity.  Once 
      outside the cell, these compounds take on new roles as intercellular 
      signaling molecules that elicit a broad spectrum of physiological 
      responses through the activation of numerous cell surface receptor 
      subtypes.  This review summarizes recent advances in the molecular 
      characterization of ATP receptors and discusses roles for cloned 
      receptors in established and novel physiological processes.
AA    N
EA    Y
LG    eng
PT    REVIEW
RF    112
IN    1081-0706  
SC    CQ: BIOCHEMISTRY AND MOLECULAR BIOLOGY.  DR: CELL BIOLOGY.  HY: 
      DEVELOPMENTAL BIOLOGY.
GA    VY428 (For ordering reprints from ISI)
KW    PURINERGIC RECEPTORS;  LIGAND-GATED ION CHANNELS;  SYNAPTIC 
      TRANSMISSION;  APOPTOSIS
KP    SMOOTH-MUSCLE CELLS;  GATED ION CHANNELS;  VASCULAR ENDOTHELIAL-CELLS;  
      EPITHELIAL NA+ CHANNEL;  RAT VAS-DEFERENS;  CYSTIC-FIBROSIS;  ATP 
      RECEPTOR;  SYNAPTIC TRANSMISSION;  FUNCTIONAL EXPRESSION;  
      GLUTAMATE-RECEPTOR

CP    Copyright US/Pacific, Current Contents(tm) from ISI, all rights reserved.

   Document 9 of 14
AU    CONIGRAVE-A-D*;  JIANG-L
TI    REVIEW - CA2+-MOBILIZING RECEPTORS FOR ATP AND UTP
AD    *UNIV SYDNEY, DEPT BIOCHEM G08, SYDNEY, NSW 2006, AUSTRALIA
CY    AUSTRALIA
SO    CELL CALCIUM, vol. 17, issue 2,  (FEB, 1995) : pp. 111-119.
SB    LifeSci
WK    03/12/1995
AB    Extracellular nucleotides are potent Ca2+ mobilizing agents, A variety 
      of receptors for extracellular ATP are recognised.  Some are involved 
      in fast neuronal transmission and operate as ligand-gated ion channels. 
      Others are involved in the paracrine or autocrine modulation of cell 
      function.  Many receptors of this type are coupled to 
      phosphoinositide-specific phospholipase C and, in some cases, other 
      phospholipases.  One of these receptors (P-2z), however, also appears 
      to operate, at least in part, as a ligand-gated ion channel.  
      Pharmacological data suggest that one nucleotide receptor subtype 
      (currently designated P-2U) responds selectively to either a purine 
      nucleotide, ATP, or a pyrimidine nucleotide, UTP. According to an 
      alternative view, ATP and UTP recognise distinct receptors.  Because of 
      the diversity of receptors for extracellular nucleotides this may be 
      the case in some cells.  Nevertheless, a G-protein coupled receptor 
      that confers both ATP and UTP sensitivity has been cloned, expressed in 
      cultured cell lines and sequenced.  This receptor appears to have two 
      ligand binding domains that may partially overlap.  The nature of this 
      overlap is discussed and a simple model presented. Activation of the 
      receptor protein via one or other ligand binding domain may underlie 
      some of the more subtle differences between the effects of ATP and UTP.
AA    N
EA    Y
LG    eng
PT    REVIEW
RF    73
IN    0143-4160  
SC    DR: CELL BIOLOGY.
GA    QH397 (For ordering reprints from ISI)
KP    INOSITOL PHOSPHOLIPID BREAKDOWN;  RENAL MESANGIAL CELLS;  PAROTID 
      ACINAR-CELLS;  SMOOTH-MUSCLE CELLS;  EXTRACELLULAR ATP;  HL60 CELLS;  
      G-PROTEINS;  P2-PURINERGIC RECEPTORS;  PYRIMIDINE NUCLEOTIDES;  
      HUMAN-NEUTROPHILS

   Document 13 of 14
AU    MOSQUEDAGARCIA-R*
TI    ADENOSINE AS A THERAPEUTIC AGENT
AD    VANDERBILT UNIV, MED CTR, SCH MED, DEPT MED, DIV CLIN PHARMACOL, 
      NASHVILLE, TN  37232
      VANDERBILT UNIV, MED CTR, SCH MED, DEPT OBSTET & GYNECOL, NASHVILLE, TN 
      37232
ZP    37232
CY    USA
SO    CLINICAL AND INVESTIGATIVE MEDICINE-MEDECINE CLINIQUE ET EXPERIMENTALE, 
      vol. 15, issue 5,  (OCT, 1992) : pp. 445-455.
SB    LifeSci;  ClinMed
WK    01/01/1992
AB    Adenosine, an endogenous nucleoside has been recently approved for use 
      in the treatment of paroxysmal supraventricular tachycardia. Adenosine 
      is nearly 100% effective in terminating tachycardia in which the 
      atrioventricular node forms part of the reentrant circuit.  Although 
      most ventricular tachycardias are insensitive to adenosine, this 
      substance is effective in ventricular tachycardia induced by 
      catecholamines or exercise.  An intravenous bolus dose of 6 mg is the 
      initial dose.  If no effect is noted a further bolus of 12 mg can be 
      given.  The most common side effects are dyspnea, chest pressure and 
      facial flushing.  This article reviews, in addition, some of the 
      comparative trials with verapamil and adenosine triphosphate, some of 
      the additional therapeutic indications, the possible mechanisms of 
      action in cardiac tissue, and the type of purinergic receptors involved 
      in the antiarrhythmic effects of adenosine.
AA    N
EA    Y
LG    eng
PT    REVIEW
RF    71
IN    0147-958X  
SC    QA: MEDICINE, RESEARCH AND EXPERIMENTAL.
GA    KB547 (For ordering reprints from ISI)
KP    PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA;  SUPRA-VENTRICULAR 
      TACHYCARDIA;  CORONARY-ARTERY DISEASE;  GUINEA-PIG;  
      ATRIOVENTRICULAR-CONDUCTION;  INTRAVENOUS ADENOSINE;  NORMOTENSIVE 
      RATS;  ACUTE MANAGEMENT;  CONSCIOUS MAN;  SINUS NODE

-- 
Terrence Brannon * brannon at lnc.usc.edu * http://lnc.usc.edu/~brannon
USC, HNB, 3614 Watt Way, Los Angeles, CA 90089-2520 * (213) 740-3397
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