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Visualization of renal microcirculation and pharmacological analysis of renal vascular responses to vasoconstrictor peptide

Visualization of renal microcirculation and pharmacological analysis of renal vascular responses to vasoconstrictor peptide
肾微循环的可视化和肾血管对缩血管肽反应的药理学分析
批准号:
08672621
负责人:
MIURA Katsuyuki
金额:
$1.54万
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:
1996
资助国家:
日本
项目状态:
已结题
起止时间:
1996 至 1998

项目摘要

项目成果

MIURA Katsuyuki的其他基金

相关文献

中文摘要
翻译
肾小球滤过率由肾小球前和肾小球后阻力血管的张力平衡决定。前者包括小叶间动脉和输入小动脉,后者包括输出小动脉。因此,直接显示肾脏微血管将有助于我们了解肾小球滤过的控制。为了直接观察这些血管,我们建立了一个由活体显微镜、CCD摄像机、视频监视器、记录器和动物室组成的光学系统,用于透照在体积水大鼠肾脏。利用该系统,可在放大2,500倍的视频监视器上显示积水肾的肾皮质微循环。局部应用内皮素异肽及其类似物可引起ETA和ETB受体参与的小叶间动脉、输入小动脉和输出小动脉的收缩。目前,我们正在开发一种连续测量系统, ...更多信息 肾微血管的红细胞速度,从而可以测量单个肾小球血流量。在本研究项目中,除了肾脏微循环的显微镜检查外,我们还进行了实验,以阐明内皮素和腺苷在整个器官水平上控制肾脏循环中的作用。结果提示,内源性ET激活ETB受体对ETA介导的肾血管收缩起生理性制动作用,这种作用显然是通过刺激一氧化氮和/或血管舒张性前列腺素释放介导的。我们还发现,肾腺苷A2受体的激活对肾小球滤过没有影响,尽管显着的肾血管舒张,表明血管舒张的传入和传出小动脉。尽管脂肪酸β-氧化的抑制剂4-戊烯酸显著刺激肾产生腺苷并降低肾小球滤过率,但腺苷A1受体不参与4-戊烯酸诱导的肾小球滤过率下降。少
英文摘要
Glomerular filtration rate is determined by the balance of the tone of pre-glomerular and post-glomerular resistance vessels. The former includes interlobular artery and afferent arteriole and the latter efferent arteriole. Therefore, direct visualization of renal microvessels would help us to learn the control of glomerular filtration. In order to visualize these vessels directly, we have constructed optic system that consisted of a vital microscopy, CCD camera, video monitor, recorder and animal chamber suitable for transillumination of hydronephrotic rat kidney in vivo. By using this system, renal cortical microcirculation of hydronephrotic kidney can be visualized on the video-monitor at the magnification of 2,500-fold. Local application of endothelin isopeptide and analog elicited vasoconstriction of interlobular artery, afferent arteriole and the efferent arteriole where both ETA and ETB receptors were involved. Currently, we are developing a system for continuous measurement of … More erythrocyte velocity of renal microvessel, thereby single glomerular blood flow can be measured. In this research project, in addition to the microscopic examination of renal microcirculation, we also performed experiments to elucidate the role of endothelin and adenosine in the control of renal circulation at the whole organ level. The results suggested that activation of ETB receptors by endogenous ET acts as a physiological brake for the ETA-mediated renal vasoconstriction, and this effect is apparently mediated by stimulation of nitric oxide and/or vasodilatoiy prostaglandin(s) release. We also found that activation of renal adenosine A2 receptor had no effect on glomerular filtration despite marked renal vasodilatation, suggesting vasodilation of both afferent and efferent arteriole. Although 4-pentenoic acid, an inhibitor of fatty acid beta- oxidation, markedly stimulated renal production of adenosine and reduced glomerular filtration rate, adenosine Al receptor was not involved in the 4-pentenoic acid-induced fall in glomerular filtration rate. Less
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Comparison Western Japan with Eastern Japan about the cause of asymptomatic cerebrovascular disorders and hippocampal atrophy in general Japanese men
  • 批准号:
    23249036
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
  • 资助金额:
    $30.2万
  • 财政年份:
    2011
  • 负责人:
    MIURA Katsuyuki
  • 依托单位:
Role of macrophages in the development and repair of renal injury
  • 批准号:
    21590600
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $3.0万
  • 财政年份:
    2009
  • 负责人:
    MIURA Katsuyuki
  • 依托单位:
Long-term changes of nutrients intake and changes of cardiovascular risk factors
  • 批准号:
    20390188
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $10.9万
  • 财政年份:
    2008
  • 负责人:
    MIURA Katsuyuki
  • 依托单位:
Nutritional factors relating to long-term change in cardiovascular risk factors
  • 批准号:
    18390199
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $6.78万
  • 财政年份:
    2006
  • 负责人:
    MIURA Katsuyuki
  • 依托单位: