Tucker B J, Blantz R C
Kidney Int. 1984 Aug;26(2):112-21. doi: 10.1038/ki.1984.144.
Furosemide, a potent diuretic, has also been shown (1) to inhibit or reduce tubuloglomerular feedback activity, (2) act as a vasodilatory agent, and (3) exhibit a modest carbonic anhydrase inhibitory effect, which could potentially reduce proximal tubule reabsorption. If furosemide can inhibit tubuloglomerular feedback as well as cause vasodilation, then glomerular filtration rate (GFR) should increase through alterations in the dynamics of glomerular ultrafiltration. The effect of acute furosemide infusion (4 mg/kg of body wt per hour) on glomerular and tubular dynamics was examined in Munich-Wistar rats by two protocols: The first allowed a 3% volume depletion (based on body wt) to occur as a result of furosemide administration (group 1); the second allowed a complete replacement of volume after furosemide administration (group 2). The results demonstrated that when volume status was maintained after furosemide administration, the nephron filtration rate remained constant (35 +/- 3 vs. 33 +/- 2 nl/min, NS) despite a twofold increase in distal flow rate (5 +/- 1 vs. 10 +/- 1 nl/min, P less than 0.01), indicating an inhibition or suppression of the tubuloglomerular feedback system. With either protocol, furosemide administration did not alter total nephron vascular resistance and nephron blood flow (190 +/- 17 vs. 200 +/- 15 ml/min); however, the afferent arteriolar resistance did decrease in rats in which volume status was maintained. Finally, with volume status maintained, we were not able to demonstrate a reduction in absolute proximal fluid reabsorption despite a 7 mm Hg increase in interstitial hydrostatic pressure (4 +/- 1 to 11 +/- 1 mm Hg, P less than 0.01) and no compensatory increase in interstitial oncotic pressure. These data indicate that tubuloglomerular feedback was inhibited but that GFR was not increased. Major changes occurred in interstitial pressures and interstitial volume after furosemide administration, but absolute proximal reabsorption remained constant.
速尿是一种强效利尿剂，研究表明它还具有以下作用：（1）抑制或降低肾小管-肾小球反馈活性；（2）作为血管扩张剂；（3）表现出适度的碳酸酐酶抑制作用，这可能会减少近端小管重吸收。如果速尿能抑制肾小管-肾小球反馈并引起血管舒张，那么肾小球滤过率（GFR）应该会通过改变肾小球超滤动力学而增加。通过两种方案研究了急性输注速尿（每小时4mg/kg体重）对慕尼黑-威斯塔大鼠肾小球和肾小管动力学的影响：第一种方案中，速尿给药导致3%的血容量减少（基于体重）（第1组）；第二种方案中，速尿给药后血容量完全恢复（第2组）。结果表明，速尿给药后维持血容量状态时，尽管远端流速增加了两倍（5±1对10±1nl/min，P<0.01），肾单位滤过率仍保持恒定（35±3对33±2nl/min，无显著性差异），这表明肾小管-肾小球反馈系统受到抑制。无论采用哪种方案，速尿给药均未改变总肾单位血管阻力和肾单位血流量（190±17对200±15ml/min）；然而，在维持血容量状态的大鼠中，入球小动脉阻力确实降低了。最后，在维持血容量状态的情况下，尽管间质静水压升高了7mmHg（4±1至11±1mmHg，P<0.01）且间质胶体渗透压没有代偿性增加，但我们未能证明绝对近端液体重吸收减少。这些数据表明肾小管-肾小球反馈受到抑制，但GFR并未增加。速尿给药后间质压力和间质容积发生了重大变化，但绝对近端重吸收保持恒定。
