Tubuloglomerular feedback and SNGFR autoregulation in the rat.
Tubuloglomerular feedback and SNGFR autoregulation in the rat.
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大鼠肾小球反馈和 SNGFR 自动调节。
DOI：
10.1152/ajprenal.1984.247.2.f267
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Moore,LC
中科院分区：
文献类型：
--
作者：
Moore,LC
进行实验和模拟研究，以检查过滤动力学状态对单个肾单位肾小球滤过率（SNGFR）自动调节的影响，以验证肾小管肾小球反馈（TGF）抑制过程中部分自动调节的存在，并确定肾小管重吸收的微小变化是否可以增强TGF在自动调节过程中调节SNGFR的能力。在水缺乏大鼠中的实验研究揭示了在TGF抑制期间肾小球毛细血管压力（使用停流法）和SNGFR的部分自动调节以及具有功能性TGF的完整SNGFR自动调节。随着动脉压升高，在远端测量中观察到体积重吸收分数小幅显著降低。肾小球滤过数学模型的结果表明，在表现出滤过压平衡而不是滤过压不平衡的动物中，SNGFR本质上对动脉压变化更敏感。这些数据和模拟结果提供了额外的支持存在一个TGF-独立的自动调节机制，似乎是一个固有的属性肾小球前血管。最后，一个简单的控制系统模型的自动调节分析表明，在近端小管或亨利体积重吸收环的小变化可以提供一些或所有的刺激TGF激活，从而显着增加的能力，TGF稳定SNGFR在动脉压上升的反应。
Experimental and simulation studies were undertaken to examine what influence the state of filtration dynamics has on single nephron glomerular filtration rate (SNGFR) autoregulation, to verify the presence of partial autoregulation during tubuloglomerular feedback (TGF) inhibition, and to determine whether small changes in tubular reabsorption could enhance the ability of TGF to regulate SNGFR during autoregulation. The experimental studies in hydropenic rats revealed partial autoregulation of glomerular capillary pressure (using the stop-flow method) and SNGFR during TGF inhibition and complete SNGFR autoregulation with functional TGF. A small significant decrease in fractional volume reabsorption was observed in the distal measurements with increased arterial pressure. Results from a mathematical model of glomerular filtration suggest that SNGFR is inherently more sensitive to changes in arterial pressure in animals exhibiting filtration pressure equilibrium rather than filtration pressure disequilibrium. These data and the simulation results provide additional support for the existence of a TGF-independent autoregulatory mechanism that appears to be an intrinsic property of the preglomerular vasculature. Finally, analysis of autoregulation with a simple control-system model suggests that small changes in proximal tubule or loop of Henle volume reabsorption can provide some or all of the stimulus for TGF activation, thereby significantly increasing the ability of TGF to stabilize SNGFR in response to a rise in arterial pressure.