Karlsen F M, Andersen C B, Leyssac P P, Holstein-Rathlou N H
Department of Medical Physiology, The Panum Institute, University of Copenhagen, Denmark.
Hypertension. 1997 Oct;30(4):975-83. doi: 10.1161/01.hyp.30.4.975.
The Dahl salt-sensitive (Dahl S) rat develops hypertension and renal injuries when challenged with a high salt diet and has been considered to be a model of chronic renal failure. Renal injuries appear very early in life compared with the spontaneously hypertensive rat (SHR). During the course of hypertension, a gradual impairment of autoregulatory control of renal blood flow might expose the glomerular circulation to periods of elevated pressure, resulting in renal injuries in Dahl S rats. Dynamic autoregulatory capacity was assessed in Dahl S and Dahl salt-resistant (Dahl R) rats, SHR, and Sprague-Dawley rats by inducing broad-band fluctuations in the arterial blood pressure and simultaneously measuring renal blood flow. Dynamic autoregulation was estimated by the transfer function using blood pressure as the input and renal blood flow as the output. Renal morphological injuries were evaluated in Dahl S rats and SHR and were scored semiquantitatively. Dynamic autoregulation was efficient and comparable in the low-frequency range (<0.015 Hz) in Dahl R rats, SHR, and Sprague-Dawley rats. The response in Dahl S rats depended strongly on the initiation time of the high salt diet. Autoregulation was preserved during a low salt diet and in rats exposed to a late-onset hypertension of short duration, only partly preserved if the late-onset hypertension was of a longer duration, and abolished in early-onset hypertension. All Dahl S rats on a high salt diet showed severe morphological changes in the kidney. In conclusion, autoregulatory capacity in the kidney of Dahl S rats is gradually impaired when rats are rendered hypertensive with a high salt diet. Renal morphological injuries develop before loss of dynamic autoregulation. Impaired autoregulation appears to be the result, not the cause, of the process that ultimately leads to renal failure in the Dahl S rat.
对盐敏感的 Dahl（Dahl S）大鼠在接受高盐饮食刺激时会出现高血压和肾损伤，被认为是慢性肾衰竭的模型。与自发性高血压大鼠（SHR）相比，肾损伤在生命早期就出现了。在高血压病程中，肾血流自动调节控制的逐渐受损可能会使肾小球循环暴露于压力升高的时期，从而导致 Dahl S 大鼠出现肾损伤。通过诱导动脉血压的宽带波动并同时测量肾血流，评估了 Dahl S 和盐抵抗性 Dahl（Dahl R）大鼠、SHR 以及 Sprague-Dawley 大鼠的动态自动调节能力。动态自动调节通过以血压为输入、肾血流为输出的传递函数来估计。对 Dahl S 大鼠和 SHR 的肾形态损伤进行了评估并进行半定量评分。在 Dahl R 大鼠、SHR 和 Sprague-Dawley 大鼠中，低频范围（<0.015 Hz）内的动态自动调节是有效的且具有可比性。Dahl S 大鼠的反应强烈依赖于高盐饮食的起始时间。在低盐饮食期间以及暴露于短期迟发性高血压的大鼠中，自动调节得以保留；如果迟发性高血压持续时间较长，则仅部分保留；而在早发性高血压中则被消除。所有接受高盐饮食的 Dahl S 大鼠肾脏均出现严重的形态学改变。总之，当用高盐饮食使 Dahl S 大鼠患高血压时，其肾脏的自动调节能力会逐渐受损。肾形态学损伤在动态自动调节丧失之前就已出现。自动调节受损似乎是最终导致 Dahl S 大鼠肾衰竭这一过程的结果，而非原因。
