Zatz R, Fujihara C K, Marcondes M
Braz J Med Biol Res. 1986;19(3):429-38.
Normal (N) rats and rats with nephrotoxic serum nephritis (NSN) were used in whole-kidney and micropuncture studies while being kept euvolemic by homologous plasma infusion and after isotonic volume expansion (VE). During euvolemia, whole kidney and single nephron (SN) glomerular filtration rate (GFR), as well as urinary sodium excretion (UNa X V), were significantly lower in NSN rats (GFR = 0.40 +/- 0.06 ml/min; SNGFR = 14.4 +/- 1.9 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min) than in controls (GFR = 1.14 +/- 0.06 ml/min; SNGFR = 32.7 +/- 2.0 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min); fractional proximal and "distal" (beyond the proximal convoluted tubule) sodium reabsorption rates were significantly higher than N, further depressing urinary sodium output. Saline expansion significantly elevated GFR and decreased renal vascular resistance (RVR) in both N and NSN rats. In the latter, however, GFR remained below, and RVR above, levels observed in N rats. Urinary sodium excretion increased markedly with saline expansion in N rats, reaching 26.9 +/- 1.31 microEq/min. NSN rats exhibited a blunted natriuretic response to expansion (UNa X V = 3.85 +/- 1.02 microEq/min); however, despite a still depressed GFR and increased RVR, urinary sodium excretion in NSN rats reached levels well above euvolemic control. Fractional proximal and "distal" tubular sodium reabsorption rates were depressed by VE in both N and NSN rats. However, this depression was less evident in NSN rats, particularly in the "distal" nephron, suggesting that the stimulus for sodium reabsorption in these segments was somehow enhanced in NSN rats. Fractional potassium excretion was increased to a much greater extent in NSN than in N rats. This finding, associated with the small depression of fractional sodium reabsorption in the "distal" nephron of NSN rats, suggests a participation of elevated levels of circulating aldosterone in the sodium retention observed in this model.
正常（N）大鼠和患有肾毒性血清性肾炎（NSN）的大鼠用于全肾和微穿刺研究，在通过同源血浆输注维持血容量正常以及等渗容量扩张（VE）后进行研究。在血容量正常期间，NSN大鼠的全肾和单肾单位（SN）肾小球滤过率（GFR）以及尿钠排泄（UNa×V）显著低于对照组（GFR = 0.40±0.06 ml/分钟；SNGFR = 14.4±1.9 nl/分钟；UNa×V = 0.05±0.02微当量/分钟）（对照组GFR = 1.14±0.06 ml/分钟；SNGFR = 32.7±2.0 nl/分钟；UNa×V = 0.05±0.02微当量/分钟）；近端和“远端”（超过近端曲管）钠重吸收率显著高于正常大鼠，进一步降低了尿钠排出量。盐水扩容显著提高了N大鼠和NSN大鼠的GFR并降低了肾血管阻力（RVR）。然而，在NSN大鼠中，GFR仍低于N大鼠，而RVR高于N大鼠。在N大鼠中，盐水扩容使尿钠排泄显著增加，达到26.9±1.31微当量/分钟。NSN大鼠对扩容的利钠反应减弱（UNa×V = 3.85±1.02微当量/分钟）；然而，尽管GFR仍然降低且RVR增加，但NSN大鼠的尿钠排泄达到远高于血容量正常时对照组的水平。在N大鼠和NSN大鼠中，VE均降低了近端和“远端”肾小管钠重吸收率。然而，这种降低在NSN大鼠中不太明显，尤其是在“远端”肾单位，这表明NSN大鼠中这些节段钠重吸收的刺激因素在某种程度上增强了。NSN大鼠中钾排泄分数的增加幅度远大于N大鼠。这一发现与NSN大鼠“远端”肾单位钠重吸收分数的小幅降低相关，提示循环中醛固酮水平升高参与了该模型中观察到的钠潴留。
