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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

基本信息

批准号：
16500258
负责人：
KAWATANI Masahito
金额：
$ 2.3万
依托单位：
Akita University
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
起止时间：
2004 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-16500258/
关键词：
Urothelium α_<1D> Receptor EP_1 Receptor Primary afferent Unit recording Primary afferent Unit recording α_<1D> Receptor 求心性線維プロスタグランジン EP1受容体 α1受容体 ATP 膀胱炎

项目摘要

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.

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释放神经递质。本研究旨在确定<1D>大鼠膀胱尿道是否有α-肾上腺素能受体的表达，以及抑制这些受体是否影响反射性排尿。雌性Wistar大鼠用于实验。通过Western blot评估受体表达。受体激活的影响进行了研究，使用膀胱测压，测量ATP浓度在膀胱腔和传入神经记录。α_受体<1D>拮抗剂萘哌地尔（0.75- 1.66mg/kg）经颈外静脉给药。采用<1D>Westernblot和免疫组织化学方法检测尿路上皮组织中α肾上腺素能受体的表达。α_<1D>受体拮抗剂萘哌地尔使清醒大鼠膀胱收缩间期延长（ICI为对照组的143%），并抑制膀胱灌注醋酸（0.1%）对ICI的兴奋作用（220%）。萘哌地尔抑制膀胱扩张（32.0%）或醋酸灌注（30.4%）引起的膀胱传入神经活动，并降低膀胱扩张时膀胱灌注液中ATP水平（36.6%）。内源性儿茶酚胺可能作用于尿道的α_<1D>受体，促进膀胱机械敏感的传入神经活动和反射性排尿。