Rector F C, Sellman J C, Martinez-Maldonado M, Seldin D W
J Clin Invest. 1967 Jan;46(1):47-56. doi: 10.1172/JCI105510.
The mechanism by which expansion of extracellular fluid volume with isotonic saline suppresses reabsorption in the proximal tubule was studied in rats by examining the relations among glomerular filtration rate (GFR), absolute and fractional reabsorption of filtrate, intrinsic reabsorptive capacity (rate of reabsorption per unit tubular volume), transit time, and tubular volume. Saline infusions reduced the per cent of the glomerular filtrate reabsorbed in the proximal tubule from 50% during antidiuresis to 25% during saline diuresis. The suppression of proximal reabsorption was the result of two factors: 1) a 30% reduction of intrinsic reabsorptive capacity, and 2) a 26% reduction of tubular volume per unit GFR.GFR invariably rose during saline diuresis. However, prevention of the rise in GFR by aortic clamping had no effect on either the inhibition of intrinsic reabsorptive capacity or the reduction in tubular volume per unit GFR produced by saline infusions. Expansion of extracellular fluid volume with isotonic saline, therefore, depressed intrinsic reabsorptive capacity and tubular volume per unit GFR by some mechanism completely independent of GFR. The effects of furosemide administration were contrasted with those of saline infusions. Furosemide inhibited intrinsic reabsorptive capacity by 40% but had no significant effect on proximal fractional reabsorption. The failure to suppress fractional reabsorption was the consequence of a disproportionate rise in tubular volume (relative to GFR) that was sufficient to completely overcome the inhibition of intrinsic reabsorptive capacity. Inhibition of intrinsic reabsorptive capacity alone, therefore, will not result in a net suppression of reabsorption of filtrate in the proximal tubule. We concluded that, although intrinsic reabsorptive capacity was inhibited during saline diuresis, the critical factor responsible for translating this inhibition into effective net suppression of proximal reabsorption was the observed reduction in tubular volume per unit GFR.
通过检测肾小球滤过率(GFR)、滤液的绝对重吸收量和重吸收率、固有重吸收能力(单位肾小管容积的重吸收速率)、转运时间和肾小管容积之间的关系,在大鼠中研究了用等渗盐水扩充细胞外液量抑制近端肾小管重吸收的机制。盐水输注使近端肾小管重吸收的肾小球滤液百分比从抗利尿期间的50%降至盐水利尿期间的25%。近端重吸收的抑制是两个因素的结果:1)固有重吸收能力降低30%,2)单位GFR的肾小管容积降低26%。盐水利尿期间GFR总是升高。然而,通过主动脉夹闭防止GFR升高对盐水输注所产生的固有重吸收能力抑制或单位GFR的肾小管容积减少均无影响。因此,用等渗盐水扩充细胞外液量通过某种完全独立于GFR的机制降低了固有重吸收能力和单位GFR的肾小管容积。将呋塞米给药的效果与盐水输注的效果进行了对比。呋塞米使固有重吸收能力抑制40%,但对近端重吸收率无显著影响。未能抑制重吸收率是肾小管容积(相对于GFR)不成比例升高的结果,这种升高足以完全克服固有重吸收能力的抑制。因此,仅抑制固有重吸收能力不会导致近端肾小管滤液重吸收的净抑制。我们得出结论,尽管在盐水利尿期间固有重吸收能力受到抑制,但将这种抑制转化为近端重吸收有效净抑制的关键因素是观察到的单位GFR的肾小管容积减少。