Role of the renal medulla in volume and arterial pressure regulation
Role of the renal medulla in volume and arterial pressure regulation
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DOI：
10.1152/ajpregu.1997.273.1.r1
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发表时间：
1997-07-01
影响因子：
2.8
通讯作者：
Cowley, AW
中科院分区：
文献类型：
--
作者：
Cowley, AW
最初对肾脏髓质循环的迷恋是由直血管毛细血管循环的独特结构所驱动的，Berliner和他的同事(Berliner， R. W .， N. G. Levinsky， D. G. Davidson和M. Eden。点。J. Med. 24: 730-744, 1958)证明可以提供逆流交换的经济性，以浓缩大量血液滤液并产生少量浓缩尿液。我们现在相信我们发现了肾髓循环的另一个同样重要的功能。数据表明，确实是100年前Starling定义的力通过肾灌注压力的变化传递到血管直肠循环的压力-钠尿机制负责。尽管仅接受肾总血流量的5-10%，但流向肾脏这一区域的血流量增加会导致肾髓质尿素梯度的冲洗和肾间质液压力的升高。这些力减少了钠和水的管状再吸收，导致尿钠和利尿。斯塔林的许多内在化学物质，他称之为“激素”，通过改变这些反应发生的动脉压的敏感性和范围，重要地调节了这种压力-钠尿反应。肾髓质的血管系统对这些血管活性药物非常敏感。最后，我们发现肾髓质循环可以通过建立压力-尿钠关系的斜率和设定点，在确定实现长期液体和电解质稳态所需的动脉压力水平方面发挥重要作用。肾髓质血流量明显减少而肾总血流量变化不易察觉可导致高血压的发生。许多问题仍然存在，现在很明显，这是一个非常复杂的监管体系。然而，髓质血流似乎是钠和水排泄的一个强有力的决定因素，并通过斯塔林教授100年前明确定义的物理力量向小管发出血容量和动脉压力变化的信号。
The original fascination with the medullary circulation of the kidney was driven by the unique structure of vasa recta capillary circulation, which Berliner and colleagues (Berliner, R. W, N. G. Levinsky, D. G. Davidson, and M. Eden. Am. J. Med. 24: 730-744, 1958) demonstrated could provide the economy of countercurrent exchange to concentrate large volumes of blood filtrate and produce small volumes of concentrated urine. We now believe we have found another equally important function of the renal medullary circulation. The data show that it is indeed the forces defined by Starling 100 years ago that are responsible for the pressure-natriuresis mechanisms through the transmission of changes of renal perfusion pressure to the vasa recta circulation. Despite receiving only 5-10% of the total renal blood flow, increases of blood flow to this region of the kidney cause a washout of the medullary urea gradient and a rise of the renal interstitial fluid pressure. These forces reduce tubular reabsorption of sodium and water, leading to a natriuresis and diuresis. Many of Starling's intrinsic chemicals, which he named ''hormones,'' importantly modulate this pressure-natriuresis response by altering both the sensitivity and range of arterial pressure around which these responses occur. The vasculature of the renal medulla is uniquely sensitive to many of these vasoactive agents. Finally, we have found that the renal medullary circulation can play an important role in determining the level of arterial pressure required to achieve long-term fluid and electrolyte homeostasis by establishing the slope and set point of the pressure-natriuresis relationship. Measurable decreases of blood flow to the renal medulla with imperceptible changes of total renal blood flow can lead to the development of hypertension. Many questions remain, and it is now evident that this is a very complex regulatory system. It appears, however, that the medullary blood flow is a potent determinant of both sodium and water excretion and signals changes in blood volume and arterial pressure to the tubules via the physical forces that Professor Starling so clearly defined 100 years ago.