Cell-to-cell signa transduction (cross talk) via ATP on prostate

通过前列腺上的 ATP 进行细胞间信号转导(串扰)

基本信息

  • 批准号:
    12670099
  • 负责人:
  • 金额:
    $ 1.79万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2000
  • 资助国家:
    日本
  • 起止时间:
    2000 至 2001
  • 项目状态:
    已结题

项目摘要

In this study, the effects of purinoceptor agonists on the release of endogenous noradrenaline (NA) evoked electrical field stimulation (EPS) prostate gland of the rat were examined. NA was quantified by HPLC coupled with electrochemical detection techniques. 1) There are two kind of purinoceptors (PI and P?) inhibiting NA-release on adrenergic nerve terminals in rat prostate. 2) NA evoked by high-frequency EPS (8 Hz) induces purines-release via a, receptor on effector cells. The amount of purines-release evoked by EPS was higher than that of NA-release (total purines : NA= 100 : 1). 3) Purines evoked by stimulation of a, receptor on effector cells affect prejunctional purinoceptor (PI and P?), and inhibit NA-release. 4) Inhibition of NA-release via prejunctional purinoceptors consequently induces the decreases of the tone in prostate smooth muscle. 5) These results indicate that excess NA evoked by high frequency EPS induced abundant purines-release from effector cells with excess contraction, and consequently inhibit NA- release and decrease the tone of contraction.The adrenergic nerve plays an important role in the control of prostate smooth muscle tone. It is well known that NA-release is regulated by feedback inhibition through prejunctional a2-adrenoceptors in most tissues. However, very few attempts have been made to investigate the regulation of neurotransmission through prejunctional purinoceptors in the prostate. In this investigation, we suggested the existence of transsynaptic neuromodulation by purines derived from effector cells.
本研究观察了嘌呤受体激动剂对电场刺激(EPS)大鼠前列腺释放内源性去甲肾上腺素(NA)的影响。NA通过HPLC结合电化学检测技术定量。1)嘌呤受体有两种(PI和P?)抑制大鼠前列腺肾上腺素能神经末梢的NA释放。2)高频EPS(8 Hz)诱发的NA通过效应细胞上的受体诱导嘌呤释放。EPS诱发的嘌呤释放量大于NA释放量(总嘌呤:NA= 100:1)。3)刺激效应细胞上的α 1受体诱发的嘌呤影响连接前嘌呤受体(PI和P?),并抑制NA释放。4)因此,通过连接前嘌呤受体抑制NA释放会导致前列腺平滑肌张力降低。5)这些结果表明,高频EPS诱发的过量NA引起效应细胞释放大量嘌呤,从而抑制NA的释放,降低收缩张力,肾上腺素能神经在前列腺平滑肌张力的调节中起重要作用。众所周知,在大多数组织中,NA的释放通过连接前α 2肾上腺素受体的反馈抑制来调节。然而,很少有人试图通过前列腺中的连接前嘌呤受体来研究神经传递的调节。在这项研究中,我们建议存在的跨突触的神经调节来自效应细胞的嘌呤。

项目成果

期刊论文数量(19)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Shinozuka K et al.: "Participation of ATP in cell volume regulation in the endothelium after hypotonic stress"Clinical and Experimental Pharmacology and Physiology. 28. 799-803 (2002)
Shinozuka K 等人:“ATP 参与低渗应激后内皮细胞体积调节”临床和实验药理学和生理学。
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    0
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Ishii-Nozawa R. et al.: "Participation of cAMP in the facilitatory action of APPCP on the noradrenaline release from rabbit ear artery."Life Science. 65. 2743-2753 (1999)
Ishii-Nozawa R. 等人:“cAMP 参与 APPCP 对兔耳动脉去甲肾上腺素释放的促进作用。”生命科学。
  • DOI:
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    0
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Hashimoto M.: "Hypotension induced by exercise is associated with enhanced release of adenyl purines from aged rat artery"American Journal of Physiology. 276. H970-H975 (1999)
Hashimoto M.:“运动引起的低血压与老年大鼠动脉腺嘌呤释放增强有关”《美国生理学杂志》。
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    0
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佐々木哲也 他: "血管内皮細胞のカルシウムレベルに及ぼすNicorandilの影響"Therapeutic Research. 21. 799-802 (2000)
Tetsuya Sasaki 等人:“尼可地尔对血管内皮细胞钙水平的影响”治疗研究 21. 799-802 (2000)。
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    0
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SHINOZUKA Kazumasa其他文献

SHINOZUKA Kazumasa的其他文献

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{{ truncateString('SHINOZUKA Kazumasa', 18)}}的其他基金

Protective participation of ATP/adenosine axis on the dilated cardiomyopathy of the life-style related diseases model animal.
ATP/腺苷轴对生活方式相关疾病模型动物扩张型心肌病的保护作用。
  • 批准号:
    21590296
  • 财政年份:
    2009
  • 资助金额:
    $ 1.79万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Does ATP / adenosine system protect sympathetic nerve of an ischemic heart in life-style related diseases model rat?
ATP/腺苷系统是否能保护生活方式相关疾病模型大鼠缺血心脏的交感神经?
  • 批准号:
    19590263
  • 财政年份:
    2007
  • 资助金额:
    $ 1.79万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Study on regulatory system of vascular permeability by ATP (Aim at pharmacological DDS)
ATP调节血管通透性系统的研究(针对药理DDS)
  • 批准号:
    16590211
  • 财政年份:
    2004
  • 资助金额:
    $ 1.79万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Participation of calcium ion in ATP release from the vascular endothelial cells.
钙离子参与血管内皮细胞释放 ATP。
  • 批准号:
    09670112
  • 财政年份:
    1997
  • 资助金额:
    $ 1.79万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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Molecular mechanisms for induction of DNA methylation by testosterone overdose in the rat prostate
大鼠前列腺中睾酮过量诱导 DNA 甲基化的分子机制
  • 批准号:
    23501263
  • 财政年份:
    2011
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Development Estrogenization of the Rat Prostate Gland
大鼠前列腺的发育雌激素化
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    2010
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    $ 1.79万
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Employing the rat prostate as a model for pseudomonas aeruginosa infections at mucosal surfaces
使用大鼠前列腺作为粘膜表面铜绿假单胞菌感染的模型
  • 批准号:
    380838-2009
  • 财政年份:
    2010
  • 资助金额:
    $ 1.79万
  • 项目类别:
    Alexander Graham Bell Canada Graduate Scholarships - Doctoral
Employing the rat prostate as a model for pseudomonas aeruginosa infections at mucosal surfaces
使用大鼠前列腺作为粘膜表面铜绿假单胞菌感染的模型
  • 批准号:
    380838-2009
  • 财政年份:
    2009
  • 资助金额:
    $ 1.79万
  • 项目类别:
    Alexander Graham Bell Canada Graduate Scholarships - Doctoral
Modifying effects of a possible endocrine disrupting chemical on rat prostate carcinogenesis
可能的内分泌干扰化学物质对大鼠前列腺癌发生的影响
  • 批准号:
    11670223
  • 财政年份:
    1999
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    $ 1.79万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
RETINOIC ACID RECEPTORS IN ESTROGENIZED RAT PROSTATE
雌激素化大鼠前列腺中的视黄酸受体
  • 批准号:
    2709015
  • 财政年份:
    1999
  • 资助金额:
    $ 1.79万
  • 项目类别:
RETINOIC ACID RECEPTORS IN ESTROGENIZED RAT PROSTATE
雌激素化大鼠前列腺中的视黄酸受体
  • 批准号:
    2905179
  • 财政年份:
    1999
  • 资助金额:
    $ 1.79万
  • 项目类别:
DEVELOPMENTAL ESTROGENIZATION OF THE RAT PROSTATE
大鼠前列腺的发育雌激素化
  • 批准号:
    2859199
  • 财政年份:
    1998
  • 资助金额:
    $ 1.79万
  • 项目类别:
CHARACTERIZATION OF THE CANINE AND RAT PROSTATE
犬和​​大鼠前列腺的特征
  • 批准号:
    6105383
  • 财政年份:
    1997
  • 资助金额:
    $ 1.79万
  • 项目类别:
CHARACTERIZATION OF THE CANINE AND RAT PROSTATE
犬和​​大鼠前列腺的特征
  • 批准号:
    6296462
  • 财政年份:
    1996
  • 资助金额:
    $ 1.79万
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