UWY COBRE: NEUROPEPTIDE SIGNALING IN CONTROL OF SALT INTAKE & BLOOD PRESSURE
UWY COBRE:控制盐摄入量的神经肽信号传导
基本信息
- 批准号:7381215
- 负责人:
- 金额:$ 38.99万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2006
- 资助国家:美国
- 起止时间:2006-07-01 至 2007-06-30
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The present studies are directed at studying the brain mechanisms controlling salt intake and cardiovascular function. The brain tachykinins, substance P (SP) and neurokinin B (NKB), are implicated in the pathogenic mechanisms underlying hypertension. To further investigate the functions of SP and NKB in cardiovascular signaling, we visualized, using immunohistochemistry, the internalization of SP receptors (NK1) and NKB (NK3) receptors in the nucleus of the solitary tract following increases in blood pressure. In control animals, NK1 and NK3 receptor immunohistochemistry revealed that the recepotrs were distributed along the plasma membrane. Activation of baroreceptors was accompanied by the appearance of finely-beaded dendrites of NST neurons. This appearance is attributed to the release of SP and the internalization of the NK1 receptor. In addition, we show that activation of baroafferents results in the internalization of NK3 receptors in the NST. Exogenous injection of NK3 receptor agonists decreased the gain of the baroreflex, which was due to a suppression of parasympathetic mediated bradycardia. Collectively, these results show a functional role of two tachykinin peptides in the control of blood pressure.
该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者(PI)可能从另一个NIH来源获得主要资金,因此可以在其他CRISP条目中表示。所列机构为中心,不一定是研究者所在机构。本研究旨在研究控制盐摄入和心血管功能的脑机制。脑速激肽P物质(SP)和神经激肽B(NKB)参与高血压的发病机制。为了进一步研究SP和NKB在心血管信号传导中的功能,我们使用免疫组织化学观察了血压升高后孤束核中SP受体(NK 1)和NKB(NK 3)受体的内化。在对照动物中,NK 1和NK 3受体免疫组织化学显示受体沿着质膜分布。压力感受器的激活伴随着NST神经元的细珠状树突的出现。这种现象归因于SP的释放和NK 1受体的内化。此外,我们表明,激活的压力传入神经的结果在NST的NK 3受体的内化。外源性注射NK 3受体激动剂可降低压力反射的增益,这是由于抑制副交感神经介导的心动过缓。总的来说,这些结果显示了两种速激肽肽在血压控制中的功能作用。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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FRANCIS W FLYNN其他文献
FRANCIS W FLYNN的其他文献
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{{ truncateString('FRANCIS W FLYNN', 18)}}的其他基金
Neuropeptide regulation of neurohypophyseal function
神经肽调节神经垂体功能
- 批准号:
8206570 - 财政年份:2008
- 资助金额:
$ 38.99万 - 项目类别:
Neuropeptide regulation of neurohypophyseal function
神经肽调节神经垂体功能
- 批准号:
7748924 - 财政年份:2008
- 资助金额:
$ 38.99万 - 项目类别:
相似国自然基金
气体信号分子硫化氢对颈动脉窦压力反射感受器的调节作用及机制
- 批准号:81100181
- 批准年份:2011
- 资助金额:20.0 万元
- 项目类别:青年科学基金项目
相似海外基金
Arterial Baroreflex Control of Blood Pressure (Exercise)
动脉压力反射控制血压(运动)
- 批准号:
6744364 - 财政年份:1996
- 资助金额:
$ 38.99万 - 项目类别:
Arterial Baroreflex Control of Blood Pressure (Exercise)
动脉压力反射控制血压(运动)
- 批准号:
7088868 - 财政年份:1996
- 资助金额:
$ 38.99万 - 项目类别:
Arterial Baroreflex Control of Blood Pressure (Exercise)
动脉压力反射控制血压(运动)
- 批准号:
6616432 - 财政年份:1996
- 资助金额:
$ 38.99万 - 项目类别:
Arterial Baroreflex Control of Blood Pressure (Exercise)
动脉压力反射控制血压(运动)
- 批准号:
7015792 - 财政年份:1996
- 资助金额:
$ 38.99万 - 项目类别:
Arterial Baroreflex Control of Blood Pressure (Exercise)
动脉压力反射控制血压(运动)
- 批准号:
6897303 - 财政年份:1996
- 资助金额:
$ 38.99万 - 项目类别:
ARTERIAL BAROREFLEX CONTROL OF BLOOD PRESSURE-- EXERCISE
动脉压力反射控制血压——运动
- 批准号:
6351969 - 财政年份:1994
- 资助金额:
$ 38.99万 - 项目类别: