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Indirect evidence that purinergic modulation of perivascular adrenergic neurotransmission in the portal vein is a physiological process.

作者信息

Burnstock G, Crowe R, Kennedy C, Török J

出版信息

Br J Pharmacol. 1984 Jun;82(2):359-68. doi: 10.1111/j.1476-5381.1984.tb10770.x.

DOI:10.1111/j.1476-5381.1984.tb10770.x
PMID:6329393
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1987025/
Abstract

The effects of adenine nucleotides and nucleosides on the contractile response to perivascular nerve stimulation were compared in the isolated portal vein of rabbit, rat and guinea-pig. 2-Chloroadenosine was more potent than adenosine and ATP, which were equipotent in producing inhibition of neurogenic contractions in the rabbit and rat via prejunctional P1-purinoceptors. In contrast, neurogenic contractions of the guinea-pig portal vein were not inhibited by adenosine and were potentiated by 2-chloroadenosine and, to a lesser extent, by ATP. Fluorescence histochemical localization of quinacrine, which binds to high levels of ATP, revealed a dense perivascular nerve plexus in the portal vein of rabbit and rat but not of guinea-pig. After chemical sympathectomy, quinacrine-positive nerves persisted in the rabbit (supporting other evidence for the presence of purinergic nerves) but not in the rat (supporting other evidence for ATP as a cotransmitter in adrenergic nerves). It is concluded that a prejunctional purinergic modulatory mechanism operates in adrenergic neurotransmission in the portal vein of rabbit and rat but not guinea-pig, and it is suggested that this indicates a physiological mechanism.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c493/1987025/f249c062fbdd/brjpharm00683-0060-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c493/1987025/f249c062fbdd/brjpharm00683-0060-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c493/1987025/f249c062fbdd/brjpharm00683-0060-a.jpg

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1
Indirect evidence that purinergic modulation of perivascular adrenergic neurotransmission in the portal vein is a physiological process.
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2
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引用本文的文献

1
That was then, this is now: the development of our knowledge and understanding of P2 receptor subtypes.那是过去,现在不同了:我们对 P2 受体亚型的认识和理解的发展。
Purinergic Signal. 2021 Mar;17(1):9-23. doi: 10.1007/s11302-021-09763-0. Epub 2021 Feb 1.
2
Purinergic receptors in the splanchnic circulation.内脏循环中的嘌呤能受体。
Purinergic Signal. 2008 Sep;4(3):267-85. doi: 10.1007/s11302-008-9096-0. Epub 2008 Apr 29.
3
Stimulation of glycogenolysis by adenine nucleotides in the perfused rat liver.灌注大鼠肝脏中腺嘌呤核苷酸对糖原分解的刺激作用。

本文引用的文献

1
The interaction of quinacrine with adenine nucleotides.奎纳克林与腺嘌呤核苷酸的相互作用。
J Biol Chem. 1954 Sep;210(1):45-56.
2
Do some nerve cells release more than one transmitter?一些神经细胞会释放不止一种神经递质吗?
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Metabolism and presynaptic inhibitory activity of 2',3' and 5'-adenine nucleotides in rat vas deferens.大鼠输精管中2'、3'和5'-腺嘌呤核苷酸的代谢及突触前抑制活性
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Contribution by purines to the neurogenic response of the vas deferens of the guinea pig.嘌呤对豚鼠输精管神经源性反应的作用。
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Release of purines and noradrenaline by ouabain and potassium chloride from vascular adrenergic nerves.哇巴因和氯化钾从血管肾上腺素能神经释放嘌呤和去甲肾上腺素。
Br J Pharmacol. 1982 Dec;77(4):625-9. doi: 10.1111/j.1476-5381.1982.tb09340.x.
6
8-phenyltheophylline: a potent P1-purinoceptor antagonist.8-苯基茶碱:一种强效的P1嘌呤受体拮抗剂。
Eur J Pharmacol. 1981 Oct 15;75(1):61-4. doi: 10.1016/0014-2999(81)90346-0.
7
Effects of adenosine on [3H]norepinephrine release from perfused mesenteric arteries of SHR and renal hypertensive rats.腺苷对自发性高血压大鼠和肾性高血压大鼠灌注肠系膜动脉中[3H]去甲肾上腺素释放的影响。
Eur J Pharmacol. 1983 Feb 18;87(2-3):349-52. doi: 10.1016/0014-2999(83)90352-7.
8
Factors influencing the release of purines and norepinephrine in the rabbit portal vein.影响兔门静脉中嘌呤和去甲肾上腺素释放的因素。
Blood Vessels. 1982;19(1):30-40. doi: 10.1159/000158371.
9
Purine release from vascular adrenergic nerves by high potassium and a calcium ionophore, A-23187.高钾和钙离子载体A-23187促使血管肾上腺素能神经释放嘌呤。
J Pharmacol Exp Ther. 1980 Dec;215(3):685-90.
10
Further evidence for the purinergic inhibition of adrenergic neurotransmission in the rat portal vein.关于嘌呤能对大鼠门静脉肾上腺素能神经传递的抑制作用的进一步证据。
Acta Physiol Lat Am. 1981;31(2):93-103.