• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Neurally evoked potentiation of tonic contractions in the guinea-pig vas deferens involves adenosine receptors.豚鼠输精管中强直性收缩的神经诱发增强作用涉及腺苷受体。
J Physiol. 1991 Feb;433:163-81. doi: 10.1113/jphysiol.1991.sp018420.
2
Parasympathetic depression of vas deferens contraction in the guinea-pig involves adenosine receptors.豚鼠输精管收缩的副交感神经抑制涉及腺苷受体。
J Physiol. 1988 Dec;407:135-53. doi: 10.1113/jphysiol.1988.sp017407.
3
A1 adenosine receptor modulation of electrically-evoked contractions in the bisected vas deferens and cauda epididymis of the guinea-pig.豚鼠输精管和附睾尾部电诱发收缩的A1腺苷受体调节
Br J Pharmacol. 1998 Jul;124(5):964-70. doi: 10.1038/sj.bjp.0701909.
4
Prostaglandin E2 selectively affects purinergic transmission in guinea pig vas deferens.前列腺素E2选择性影响豚鼠输精管中的嘌呤能传递。
Neuropharmacology. 1991 Oct;30(10):1107-12. doi: 10.1016/0028-3908(91)90140-7.
5
A comparison of the effects of exogenous and endogenous prostaglandins on fast and slow contractions of field-stimulated guinea-pig vas deferens.外源性和内源性前列腺素对电场刺激的豚鼠输精管快速和慢速收缩作用的比较。
Br J Pharmacol. 1995 Nov;116(6):2679-84. doi: 10.1111/j.1476-5381.1995.tb17226.x.
6
Effects of calcium-entry modulators on the biphasic neurogenic contractions in the circular muscle of guinea pig vas deferens.钙内流调节剂对豚鼠输精管环形肌双相神经源性收缩的影响。
Jpn J Pharmacol. 1989 Jan;49(1):59-65. doi: 10.1254/jjp.49.59.
7
Evidence for the differential release of the cotransmitters ATP and noradrenaline from sympathetic nerves of the guinea-pig vas deferens.豚鼠输精管交感神经中共同递质三磷酸腺苷(ATP)和去甲肾上腺素差异释放的证据。
J Physiol. 1996 Nov 1;496 ( Pt 3)(Pt 3):731-48. doi: 10.1113/jphysiol.1996.sp021723.
8
Evidence that ATP released from the postsynaptic site by noradrenaline, is involved in mechanical responses of guinea-pig vas deferens: cascade transmission.去甲肾上腺素从突触后位点释放的ATP参与豚鼠输精管机械反应的证据:级联传递。
Neuroscience. 1992 Sep;50(2):455-65. doi: 10.1016/0306-4522(92)90437-7.
9
Release of noradrenaline and ATP by electrical stimulation and nicotine in guinea-pig vas deferens.电刺激和尼古丁对豚鼠输精管去甲肾上腺素和三磷酸腺苷的释放作用
Naunyn Schmiedebergs Arch Pharmacol. 1991 Oct;344(4):419-29. doi: 10.1007/BF00172581.
10
[Analysis of the contractions evoked by sympathetic nerve stimulation, and thermal effect on the guinea-pig vas deferens--study as a model for the thermotherapy of benign prostatic hyperplasia].[交感神经刺激诱发的收缩分析以及热对豚鼠输精管的影响——作为良性前列腺增生热疗模型的研究]
Nihon Hinyokika Gakkai Zasshi. 2000 Apr;91(4):459-68. doi: 10.5980/jpnjurol1989.91.459.

引用本文的文献

1
Physiology of the vas deferens.输精管的生理学。
World J Urol. 1994;12(5):281-5. doi: 10.1007/BF00191208.

本文引用的文献

1
Outflux of various phosphates during membrane depolarization of excitable tissues.可兴奋组织膜去极化过程中各种磷酸盐的外流。
Am J Physiol. 1962 Mar;202:469-74. doi: 10.1152/ajplegacy.1962.202.3.469.
2
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。
Eur J Pharmacol. 1981 Jan 5;69(1):41-53. doi: 10.1016/0014-2999(81)90600-2.
3
Origin of adenosine released from rat vas deferens by nerve stimulation.神经刺激引起大鼠输精管释放腺苷的来源。
Eur J Pharmacol. 1982 Apr 23;79(3-4):233-43. doi: 10.1016/0014-2999(82)90629-x.
4
High levels of neuropeptide Y in peripheral noradrenergic neurons in various mammals including man.在包括人类在内的各种哺乳动物的外周去甲肾上腺素能神经元中,神经肽Y水平较高。
Neurosci Lett. 1983 Dec 2;42(2):167-72. doi: 10.1016/0304-3940(83)90401-9.
5
Evidence that ATP acts as a co-transmitter with noradrenaline in sympathetic nerves supplying the guinea-pig vas deferens.有证据表明,在支配豚鼠输精管的交感神经中,三磷酸腺苷(ATP)作为去甲肾上腺素的共递质发挥作用。
Eur J Pharmacol. 1983 Aug 19;92(1-2):161-3. doi: 10.1016/0014-2999(83)90126-7.
6
Inhibition of excitatory junction potentials in guinea-pig vas deferens by alpha, beta-methylene-ATP: further evidence for ATP and noradrenaline as cotransmitters.α,β-亚甲基三磷酸腺苷对豚鼠输精管兴奋性接头电位的抑制作用:三磷酸腺苷和去甲肾上腺素作为共同递质的进一步证据
Eur J Pharmacol. 1984 Apr 13;100(1):85-90. doi: 10.1016/0014-2999(84)90318-2.
7
Cotransmitters in the motor nerves of the guinea pig vas deferens: electrophysiological evidence.豚鼠输精管运动神经中的共递质:电生理证据。
Science. 1982 Nov 12;218(4573):693-5. doi: 10.1126/science.6291151.
8
Presynaptic regulation of the release of catecholamines.儿茶酚胺释放的突触前调节。
Pharmacol Rev. 1980 Dec;32(4):337-62.
9
Pharmacological evidence that adenosine triphosphate and noradrenaline are co-transmitters in the guinea-pig vas deferens.三磷酸腺苷和去甲肾上腺素作为豚鼠输精管中共同递质的药理学证据。
J Physiol. 1984 Feb;347:561-80. doi: 10.1113/jphysiol.1984.sp015083.
10
Ecto-adenosine triphosphatase activity at the cholinergic nerve endings of the Torpedo electric organ.电鳐电器官胆碱能神经末梢的ecto-三磷酸腺苷酶活性
Life Sci. 1983 Dec 26;33(26):2635-41. doi: 10.1016/0024-3205(83)90347-8.

豚鼠输精管中强直性收缩的神经诱发增强作用涉及腺苷受体。

Neurally evoked potentiation of tonic contractions in the guinea-pig vas deferens involves adenosine receptors.

作者信息

Tsunoo A, Kurokawa M, Takahashi K

机构信息

Meiji Institute of Health Science, Odawara, Japan.

出版信息

J Physiol. 1991 Feb;433:163-81. doi: 10.1113/jphysiol.1991.sp018420.

DOI:10.1113/jphysiol.1991.sp018420
PMID:1841937
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1181365/
Abstract
  1. In the pelvic plexus-vas deferens preparation of the guinea-pig, conditioning stimulation of the pelvic nerves depressed the phasic component of biphasic contractions evoked by test stimulation of the hypogastric nerves, but potentiated the tonic component. 2. Similarly, in the deganglionated vas deferens preparation, conditioning stimulation applied directly to postganglionic nerves issuing from the pelvic nerve side of the pelvic plexus depressed the phasic component of biphasic contractions evoked by test stimulation of the nerves issuing from the plexus on the side of the hypogastric nerve, but potentiated the tonic component. 3. In the deganglionated preparation in the presence of alpha,beta-methylene adenosine 5'-triphosphate (alpha,beta-mATP) by which the phasic component was removed, test contractions were markedly reduced by phentolamine and prazosin, and potentiated in a manner dependent on the magnitude of conditioning stimulation. 4. In the deganglionated preparations that were persistently exposed to alpha,beta-mATP (5-10 microM), attempts were made to identify the substance(s) mediating the potentiation of the prazosin-sensitive contractions and their sites of action. 5. Noradrenaline and neuropeptide Y depressed the test contractions. 6. ATP, adenosine 5'-diphosphate, adenosine 5'-monophosphate and adenosine potentiated the contractions. Inosine and adenine were without effect. The effect of ATP was antagonized by 8-phenyltheophylline. N6-Cyclohexyladenosine (CHA) potentiated the contractions in a dose-dependent and 8-phenyltheophylline-sensitive manner. 7. The conditioning stimulation-induced potentiation of test contractions was antagonized by 8-phenyltheophylline, but was further increased by dipyridamole. 8. Methoxamine-evoked contractions were potentiated by conditioning stimulation of the nerves in a manner antagonized by 8-phenyltheophylline, and also by CHA. 9. Adenosine and CHA inhibited in an 8-phenyltheophylline-sensitive manner field stimulation-induced release of 3H-activity from deganglionated vas deferens preloaded with [3H]noradrenaline. 10. In the deganglionated preparation that was not exposed to alpha, beta-mATP, ATP-evoked contractions were potentiated by conditioning stimulation and by CHA. 11. It is indicated that conditioning stimulation and adenosine exert opposite actions on phasic and on tonic contractions in spite of the results showing that each of them postjunctionally potentiates the responses to both ATP and noradrenaline. 12. These results suggest that conditioning stimulation releases adenosine and that adenosine potentiates tonic contractions by increasing the responsiveness of the muscle to noradrenaline through the postjunctional adenosine receptors.
摘要
  1. 在豚鼠盆腔神经丛 - 输精管标本中,对盆腔神经进行条件刺激可抑制由腹下神经测试刺激诱发的双相收缩的时相成分,但增强紧张性成分。2. 同样,在去神经节的输精管标本中,直接对从盆腔神经丛盆腔神经侧发出的节后神经施加条件刺激,可抑制由从腹下神经侧神经丛发出的神经测试刺激诱发的双相收缩的时相成分,但增强紧张性成分。3. 在存在α,β - 亚甲基腺苷5'-三磷酸(α,β - mATP)从而去除时相成分的去神经节标本中,酚妥拉明和哌唑嗪可使测试收缩明显减弱,且以依赖于条件刺激强度的方式增强收缩。4. 在持续暴露于α,β - mATP(5 - 10 microM)的去神经节标本中,尝试鉴定介导哌唑嗪敏感收缩增强的物质及其作用位点。5. 去甲肾上腺素和神经肽Y可抑制测试收缩。6. ATP、腺苷5'-二磷酸、腺苷5'-单磷酸和腺苷可增强收缩。肌苷和腺嘌呤无作用。ATP的作用可被8 - 苯基茶碱拮抗。N6 - 环己基腺苷(CHA)以剂量依赖性和8 - 苯基茶碱敏感的方式增强收缩。7. 8 - 苯基茶碱可拮抗条件刺激诱导的测试收缩增强,但双嘧达莫可使其进一步增强。8. 甲氧明诱发的收缩可被神经的条件刺激以8 - 苯基茶碱拮抗的方式增强,CHA也有此作用。9. 腺苷和CHA以8 - 苯基茶碱敏感的方式抑制用[3H]去甲肾上腺素预加载的去神经节输精管的场刺激诱导的3H活性释放。10. 在未暴露于α,β - mATP的去神经节标本中,ATP诱发的收缩可被条件刺激和CHA增强。11. 结果表明,尽管条件刺激和腺苷在突触后均增强对ATP和去甲肾上腺素的反应,但它们对时相收缩和紧张性收缩的作用相反。12. 这些结果提示,条件刺激释放腺苷,且腺苷通过突触后腺苷受体增加肌肉对去甲肾上腺素的反应性来增强紧张性收缩。