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慢性容量扩张大鼠肾小球滤过率和肾血流量的调控

The control of glomerular filtration rate and renal blood flow in chronically volume-expanded rats.

作者信息

Davis J M, Häberle D A, Kawata T

机构信息

Department of Physiology, University of Munich, F.R.G.

出版信息

J Physiol. 1988 Aug;402:473-95. doi: 10.1113/jphysiol.1988.sp017216.

Abstract
  1. Chronic volume expansion by dietary salt loading practically abolishes tubuloglomerular feed-back (TGF) by means of a humoral inhibitor in tubular fluid. Elimination of the vasoconstrictor influence of feed-back does not, however, increase glomerular filtration rate (GFR) and renal blood flow (RBF), implying that chronic salt loading induces additional preglomerular vasoconstriction. This being so, the feed-back response which, although absent in free-flowing nephrons, can still be elicited by loop of Henle perfusion with Ringer solution, should be essentially normal, except that nephron GFR at any loop perfusion rate should be lower than in controls. Persistence of RBF, GFR and nephron GFR autoregulation would imply that autoregulation is achieved by a preglomerular resistance control system independent of feed-back. 2. These hypotheses were tested by clearance and micropuncture experiments in rats chronically fed a diet containing 40 g NaCl (kg food)-1. 3. RBF and GFR autoregulation indeed persisted, the former down to 90 mmHg compared with 105 mmHg in controls. In controls, nephron GFR measured distally was autoregulated down to 90 mmHg whereas that measured proximally was autoregulated only above 105 mmHg. In high-salt rats nephron GFR from both sites was autoregulated to 90 mmHg. 4. Loop of Henle perfusion with homologous tubular fluid in high-salt rats confirmed attenuation of feed-back. Loop perfusion with Ringer solution yielded a response comparable to that in controls (maximal reduction of nephron GFR to 57%, compared with 56% in controls). Absolute nephron GFR at any loop perfusion rate was lower in high-salt rats than in controls. 5. These observations confirm the initial hypotheses. Considering feed-back and autoregulation as independent, preglomerular resistance control mechanisms, together with elementary haemodynamic considerations, allows formulation of a renal haemodynamics model whose quantitative predictions regarding characteristics of RBF, GFR and feed-back control are remarkably consistent with the literature.
摘要
  1. 通过饮食中盐分负荷导致的慢性容量扩张实际上借助肾小管液中的一种体液抑制剂消除了球管反馈(TGF)。然而,消除反馈的血管收缩影响并不会增加肾小球滤过率(GFR)和肾血流量(RBF),这意味着慢性盐负荷会诱导额外的肾小球前血管收缩。既然如此,尽管在自由流动的肾单位中不存在反馈反应,但通过用林格溶液灌注亨氏袢仍可引发该反应,除了在任何袢灌注率下肾单位GFR应低于对照组外,反馈反应应基本正常。RBF、GFR和肾单位GFR自身调节的持续存在意味着自身调节是由独立于反馈的肾小球前阻力控制系统实现的。2. 通过对长期喂食含40 g NaCl(每千克食物)的大鼠进行清除率和微穿刺实验来检验这些假设。3. RBF和GFR自身调节确实持续存在,前者降至90 mmHg,而对照组为105 mmHg。在对照组中,远端测量的肾单位GFR自身调节至90 mmHg,而近端测量的仅在高于105 mmHg时才自身调节。在高盐大鼠中,两个部位的肾单位GFR均自身调节至90 mmHg。4. 用高盐大鼠的同源肾小管液灌注亨氏袢证实了反馈的减弱。用林格溶液进行袢灌注产生的反应与对照组相当(肾单位GFR最大降低至57%,而对照组为56%)。在任何袢灌注率下,高盐大鼠的绝对肾单位GFR均低于对照组。5. 这些观察结果证实了最初的假设。将反馈和自身调节视为独立的肾小球前阻力控制机制,再结合基本的血流动力学考虑因素,就可以构建一个肾血流动力学模型,其关于RBF、GFR和反馈控制特征的定量预测与文献非常一致。

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RENAL HEMODYNAMICS.肾血流动力学
Am J Med. 1964 May;36:698-719. doi: 10.1016/0002-9343(64)90181-0.
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[Use of enzymatic methods in the determination of inulin].[酶法在菊粉测定中的应用]
Klin Wochenschr. 1963 Jun 15;41:615-8. doi: 10.1007/BF01487418.
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