Antagonism by Aspirin and Fenamates of Bronchoconstriction and Nociception induced by Adenosine-5′-triphosphate

Collier, H. O. J.; James, Genevieve; Schneider, C

doi:10.1038/212411a0

Cited by 93 publications

(40 citation statements)

References 10 publications

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“…The first hints on a possible algogenic role for extracellular nucleotides date back to the 1960s, when a painful response was generated by the injection of ATP in the human blister base preparation [8] and ATP-induced pain and bronchospasm were demonstrated to be sensitive to aspirin [9].…”

Section: Extracellular Nucleotides and Pain Transmissionmentioning

confidence: 99%

P2Y purinergic receptors: New targets for analgesic and antimigraine drugs

Magni

Ceruti

2013

Biochemical Pharmacology

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Non-standard abbreviations:AR-C126313, 5-(7-chloro-4H-1-thia-3-aza-benzo[f]-4-yl)-3-methyl-6-thioxo-piperadin-2-one; AR-C67085, [[[[(2R,3S,4R,5R)-5-(6-amino-2-propylsulfanylpurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methoxy-hydroxyphosphoryl]oxy-hydroxyphosphoryl]-dichloromethyl]phosphonic acid; AR-C69931MX, [dichloro-[[[(2R,3S,4R,5R)-3,4-dihydroxy-5-[6-(2-methylsulfanylethylamino)-2-(3,3,3-trifluoropropylsulfanyl) 3-[7-[[2-(3,4-BDNF, brain-derived neurotrophic factor; BK, bradykinin; CFA, Complete Freund's adjuvant; CGRP, calcitonin gene-related peptide; DRG, dorsal root ganglia; FHM1, familial hemiplegic migraine type 1; INS37217, P(1)-(uridine 5')-P(4)-(2'-deoxycytidine 5')tetraphosphate, tetrasodium salt; INS48823, {[(3aR,4R,6R,6aR)-2-benzyl-6-(2,4-dioxo-

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Section: Extracellular Nucleotides and Pain Transmissionmentioning

confidence: 99%

P2Y purinergic receptors: New targets for analgesic and antimigraine drugs

Magni

Ceruti

2013

Biochemical Pharmacology

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“…Nonsteroidal anti-inflammatory agents antagonize some effects of bradykinin [4,14], ATP [5], SRS-A [2], SRS-C [15,16 and 17], and AA [3,8], The 'capricious' nature of this antagonism and other considerations led to the hypothesis of a common factor being released from those prep arations in which this antagonism is present [6], This hypothesis has been further substantiated by the description of RCS, proposed as a final com mon mediator sensitive to blockade by anti-inflammatory agents [6,10]. No evidence is available concerning the chemical nature of RCS of anaphylaxis, but it is very labile, disappearing rapidly after collection [10].…”

Section: Discussionmentioning

confidence: 99%

Release of Vasoactive Substances from Guinea-Pig Lungs by Slow-Reacting Substance C and Arachidonic Acid

Vargäftig¹,

Dao²

1971

Pharmacology

108

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Arachidonic acid and ‘slow-reacting substance C, perfused through isolated guinea-pig lungs, release a ‘rabbit aorta contracting substance C (RCS-C), indistinguishable from a RCS released under similar conditions by anaphylaxis, bradykinin and ‘slow-reacting substance A’. Release of RCS-C is blocked by previous perfusion of the lungs with aspirin or phenylbutazone. A role for ‘rabbit aorta contracting substances’, released during inflammation by a cascade of events initially evoked by phospholipase A activation, is suggested.

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“…The involvement of ATP in the initiation of pain was recognized early (Collier et al, 1966;Bleehen and Keele, 1977;Burnstock, 1981;Jahr and Jessell, 1983). A major advance was made when the P2X 3 ionotropic receptor was cloned in 1995 (Chen et al, 1995;Lewis et al, 1995) and shown later to be predominantly localized in the subpopulation of small nociceptive sensory nerves that label with isolectin B4 (IB4) in DRG (Bradbury et al, 1998).…”

Section: Painmentioning

confidence: 99%