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==History== |
==History== |
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Purines were first proposed as extracellular signalling molecules in |
Purines were first proposed as extracellular signalling molecules in 1929 by [[Albert Szent-Györgyi]] who observed that when purified adenine compounds were [[Injection (medicine)|injected]], they produced a temporary [[bradycardia|reduction in heart rate]].<ref>{{cite journal | author = Drury AN, Szent-Györgyi A | title = The physiological activity of adenine compounds with special reference to their effect on the mammalian heart | journal = J. Physiol. | volume = 68 | year = 1929 | pmid = 16994064 | doi = | issn = }}</ref> In 1959 [[Pamela Holton]], working at [[St Mary's Hospital, London|St Mary's Hospital]] medical school showed that ATP was released from [[sensory neuron|sensory neurons]] upon [[antidromic|antidromic stimulation]],<ref>{{cite journal | author = Holton P | title = The liberation of adenosine triphosphate on antidromic stimulation of sensory nerves | journal = J. Physiol. | volume = 145 | year = 1959 | pmid = 13642316 | doi = | issn = }}</ref> the first evidence that ATP may act as a [[neurotransmitter]]. |
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In the |
In the 1960s, the classical view of [[autonomic nervous system|autonomic]] [[smooth muscle]] control was that [[sympathetic nervous system|sympathetic neurons]] released [[noradrenaline]], whilst the responses of [[antagonist|antagonistic]] [[parasympathetic nervous system|parasympathetic neurons]] were mediated by [[acetylcholine]]. However, in a number of systems responses could still be observed in the presence of cholinergic and adrenergic blockers.<ref>{{cite journal | author = Martinson J, Muren A | title = Excitatory and inhibitory effects if vagus stimulation on gastric motility in the cat | journal = Acta Physiol. Scand. | volume = 57 | year = 1963 | pmid = | doi = | issn = }}</ref><ref>{{cite journal | author = Burnstock G, Campbell G, Bennett M, Holman ME | title = Inhibition of the smooth muscle of the taenia coli | journal = Nature | volume = 200 | year = 1963 | pmid = 14082235 | doi = | issn = }}</ref> In 1972 [[Geoffrey Burnstock]] proposed that the non-adrenergic, non-cholinergic ([[NANC]]) neurotransmitter was ATP.<ref>{{cite journal | author = Burnstock G | title = Purinergic Nerves | journal = Pharmacol. Rev. | volume = 24 | year = 1972 | pmid = 4404211 | doi = | issn = }}</ref> This proposal was met with initial criticism, since ATP was known to be a critical [[ubiquitous]] [[adenosine triphosphate#biosynthesis|intracellular molecular energy source]]<ref>Lipmann F. (1941) ''Adv. Enzymol.'' 1, 99-162.</ref> so it seemed [[counter-intuitive]] that cells might also actively release this vital molecule as a neurotransmitter. |
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Revision as of 11:33, 16 February 2009
Purinergic receptors are a super-family of membrane receptors which facilitate cellular responses in reaction to the presence of extra-cellular purines. Naturally occuring ligands for purinergic receptors are largely derivatives of adenine (ATP, ADP, and adenosine), though derivatives of uracil are also endogenous ligands.
History
Purines were first proposed as extracellular signalling molecules in 1929 by Albert Szent-Györgyi who observed that when purified adenine compounds were injected, they produced a temporary reduction in heart rate.[1] In 1959 Pamela Holton, working at St Mary's Hospital medical school showed that ATP was released from sensory neurons upon antidromic stimulation,[2] the first evidence that ATP may act as a neurotransmitter.
In the 1960s, the classical view of autonomic smooth muscle control was that sympathetic neurons released noradrenaline, whilst the responses of antagonistic parasympathetic neurons were mediated by acetylcholine. However, in a number of systems responses could still be observed in the presence of cholinergic and adrenergic blockers.[3][4] In 1972 Geoffrey Burnstock proposed that the non-adrenergic, non-cholinergic (NANC) neurotransmitter was ATP.[5] This proposal was met with initial criticism, since ATP was known to be a critical ubiquitous intracellular molecular energy source[6] so it seemed counter-intuitive that cells might also actively release this vital molecule as a neurotransmitter.
newly characterized plasma membrane molecules involved in several and as yet only partially known cellular functions such as vascular reactivity, apoptosis and cytokine secretion.
Little is known about the effect extracellular microenvironment has on their function.
Fibroblasts share several features with smooth muscle cells and are an important constituent of the atherosclerotic plaque.
This receptors have their effect of high glucose concentration on ATP-mediated responses in human fibroblasts.
The members of the family include the following:
| Name | Activation | Class |
| P1 receptors | adenosine | G protein-coupled receptors |
| P2Y receptors | nucleotides | G protein-coupled receptors |
| P2X receptors | ATP | ligand-gated ion channel |
References
- ^ Drury AN, Szent-Györgyi A (1929). "The physiological activity of adenine compounds with special reference to their effect on the mammalian heart". J. Physiol. 68. PMID 16994064.
- ^ Holton P (1959). "The liberation of adenosine triphosphate on antidromic stimulation of sensory nerves". J. Physiol. 145. PMID 13642316.
- ^ Martinson J, Muren A (1963). "Excitatory and inhibitory effects if vagus stimulation on gastric motility in the cat". Acta Physiol. Scand. 57.
- ^ Burnstock G, Campbell G, Bennett M, Holman ME (1963). "Inhibition of the smooth muscle of the taenia coli". Nature. 200. PMID 14082235.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Burnstock G (1972). "Purinergic Nerves". Pharmacol. Rev. 24. PMID 4404211.
- ^ Lipmann F. (1941) Adv. Enzymol. 1, 99-162.
External links
- IUPHAR GPCR Database - Adenosine receptors
- IUPHAR GPCR Database - P2Y receptors
- Purinergic+Receptors at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
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