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Urothelium releases neuro-like chemical substances for micturition reflex

Urothelium releases neuro-like chemical substances for micturition reflex
尿路上皮释放神经样化学物质以进行排尿反射
批准号:
16500258
负责人:
KAWATANI Masahito
金额:
$2.3万
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:
2004
资助国家:
日本
项目状态:
已结题
起止时间:
2004 至 2005

项目摘要

项目成果

KAWATANI Masahito的其他基金

相关文献

中文摘要
翻译
以往的研究表明,尿路上皮细胞α_1肾上腺素能受体的激活可释放神经递质。本研究旨在探讨大鼠膀胱尿路上皮中是否有肾上腺素能受体的表达,以及抑制这些受体是否会影响反射性排尿。实验选用雌性Wistar大鼠。免疫印迹法检测受体的表达。通过膀胱测压、膀胱腔内三磷酸腺苷浓度测定和传入神经记录来研究受体激活的影响。α-1d>拮抗剂萘哌地尔(0.75-1.66 mg/kg)静脉注入颈外静脉。免疫组织化学和免疫组织化学方法检测尿路上皮组织中肾上腺素能受体的表达。1受体拮抗剂NAFP可延长清醒大鼠持续输注膀胱测压时的收缩间期(ICI),为对照组的143%,并可抑制膀胱内注入0.1%的醋酸对ICI的兴奋作用(220%)。NAFP可抑制膀胱扩张(32.0%)或醋酸注入(30.4%)引起的膀胱传入神经活动,并降低膀胱扩张时膀胱灌流液中的ATP水平(36.6%)。内源性儿茶酚胺似乎作用于尿路上皮中的α_1d和gt;受体,以促进机械敏感型膀胱传入神经的活动和反射性排尿。
英文摘要
Previous studies revealed that activation of alpha_1 adrenergic receptors in urothelial cells releases neurotransmitters. This study was undertaken to determine if alpha_<1D> adrenergic receptors are expressed in the urothelium of the rat bladder and if inhibition of these receptors affects reflex voiding. Female Wistar rats were used for the experiments. Receptor expression was evaluated by Western blot. The effects of receptor activation were studied using cystometrograms, measurement of ATP concentrations in the bladder lumen and afferent nerve recording. The alpha_<1D> antagonist, naftopidil (0.75-1.66 mg/kg) was administered intravenously into the external jugular vein. Expression of alpha_<1D> adrenergic receptors was detected in urothelial tissue with Westernblot and Immunohistochemistry. The alpha_<1D> receptor antagonist, naftopidil prolonged the intercontraction interval (ICI, 143 % of the control) during continuous infusion cystometrograms in conscious rats, and suppressed the excitatory effect of intravesical infusion of acetic acid (0.1 %) on the ICI (220 %). Naftopidil inhibited bladder afferent nerve activity induced by bladder distension (32.0%) or acetic acid infusion (30.4 %) and reduced the ATP levels in the bladder perfusate during bladder distension (36.6 %). Endogenous catecholamines appear to act on alpha_<1D> receptors in the urothelium to facilitate the mechano-sensitive bladder afferent nerve activity and reflex voiding.
期刊论文(33)
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会议论文
Prostaglandin facilitates afferent nerve activity via EP_1 receptors during urinary bladder inflammation in rats.
前列腺素在大鼠膀胱炎症期间通过 EP_1 受体促进传入神经活动。
DOI: --
发表时间: 2006
期刊: Biomedical Res (in press)
影响因子: --
作者: [Ikeda M, Kawatani M, Maruyama T, Ishihama H]
通讯作者: Ishihama H
Effectiveness of an anti-inflammatory drug,loxoprofen,for patients with nocturia.
抗炎药洛索洛芬对夜尿症患者的疗效。
DOI: --
发表时间: 2005
期刊: Int.J Urology 12
影响因子: --
作者: [Saito M, Kawatani M, Kinoshita Y, Satoh K, Miyagawa I]
通讯作者: Miyagawa I
DOI: 10.1016/s0022-5347(05)00016-9
发表时间: 2006-01-01
期刊: JOURNAL OF UROLOGY
影响因子: 6.6
作者: [Ishihama, H, Momota, Y, Kawatani, M]
通讯作者: Kawatani, M
排尿メカニズムにおける膀胱知覚神経系の役割
膀胱感觉神经系统在排尿机制中的作用
DOI: --
发表时间: 2004
期刊: 排尿障害プラクティス 12・4
影响因子: --
作者: [河谷正仁, 中村靖夫, 百田芳春 他]
通讯作者: 百田芳春 他
共 13 条
    MECHANISMS OF BLADDER EP1THELIUM INDUCE PAIN SENSATION
    • 批准号:
      21600001
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $3.08万
    • 财政年份:
      2009
    • 负责人:
      KAWATANI Masahito
    • 依托单位:
    Molecular mechanisms of sensory svstem from urinary bladder
    • 批准号:
      08044239
    • 项目类别:
      Grant-in-Aid for international Scientific Research
    • 资助金额:
      $5.31万
    • 财政年份:
      1996
    • 负责人:
      KAWATANI Masahito
    • 依托单位:
    Mechanism of recovery of autonomic function in the pelvic ganglia following pelvic nerve transection
    • 批准号:
      06680815
    • 项目类别:
      Grant-in-Aid for General Scientific Research (C)
    • 资助金额:
      $1.41万
    • 财政年份:
      1994
    • 负责人:
      KAWATANI Masahito
    • 依托单位:
    Study of sensory mechanisms from the pelvic viscera
    • 批准号:
      04044145
    • 项目类别:
      Grant-in-Aid for international Scientific Research
    • 资助金额:
      $5.38万
    • 财政年份:
      1992
    • 负责人:
      KAWATANI Masahito
    • 依托单位: