Kövér G, Tost H
Acta Physiol Acad Sci Hung. 1978;51(1-2):41-50.
Renal function was investigated in non-hydrated normal dogs and in dogs with slight isotonic hypervolaemia before and after increasing the excreting renal mass by connecting a pair of isolated kidneys into their circulation. After connecting the isolated kidneys to the perfusor's circulation, the excreting capacity of the in situ kidneys decreased markedly in both groups, without any change in the arterial blood pressure. Their urine output calculated for 100g kidney weight dropped from 0.52 +/- 0.43 to 0.30 +/- 0.18 ml/min in the non-hydrated group, and from 2.3 +/- 1.17 to 1.33 +/- 0.96 ml/min in the hydrated one. The urine flow of the isolated kidneys was 0.29 +/- 0.12 ml/min in the non-hydrated and 1.11 +/- 0.53 ml/min in the hydrated animals. Sodium excretion displayed similar changes. The findings suggest, that the excretory capacity of the kidneys and its distribution between the two kidneys is regulated very precisely. In our opinion, one or more "natriuretic factor" may be responsible for this precise regulation. The supposed factor seems to be produced extrarenally, and is only "used up" by the kidneys. It appears to exert its effect on the tubular part of the nephron, regulating the permeability of the tubular wall and controlling in this way the reflux of sodium and water from the capillary side to the tubular lumen. The decreased excreting capacity of the kidneys is attributed to an increased consumption of the natriuretic factor by four kidneys.
在非水化正常犬以及轻度等渗性血容量过多的犬中,在通过将一对离体肾脏接入其循环系统以增加肾脏排泄量之前和之后,对其肾功能进行了研究。将离体肾脏接入灌注器循环后,两组犬的原位肾脏排泄能力均显著下降,而动脉血压无任何变化。非水化组以100g肾脏重量计算的尿量从0.52±0.43ml/min降至0.30±0.18ml/min,水化组则从2.3±1.17ml/min降至1.33±0.96ml/min。非水化动物离体肾脏的尿流量为0.29±0.12ml/min,水化动物为1.11±0.53ml/min。钠排泄也呈现类似变化。这些发现表明,肾脏的排泄能力及其在两个肾脏之间的分配受到非常精确的调节。我们认为,一种或多种“利钠因子”可能负责这种精确调节。推测的因子似乎是在肾脏外产生的,并且仅被肾脏“消耗”。它似乎对肾单位的肾小管部分发挥作用,调节肾小管壁的通透性,并以此控制钠和水从毛细血管侧反流至肾小管腔。肾脏排泄能力的下降归因于四个肾脏对利钠因子的消耗增加。