Abstract

Computer simulation of osmotic gradient without active transport in renal inner medulla. It has been generally supposed that the osmotic gradient observed in the inner medulla of mammalian kidneys during antidiuresis results from countercurrent multiplication of active sodium reabsorption from thin ascending limbs of Henle. However, disagreement persists on whether the thin ascending limb can transport sodium actively. An alternative model has been proposed by Kokko and Rector. In this model water reabsorption from the descending limb of Henle creates a high tubular concentration of sodium at the bend of the loop, so that sodium can move passively out of the ascending thin limb. The present report shows that computer simulation of this model can indeed result in an osmotic gradient in the inner medulla, on condition that sodium movement out of the thin ascending limb results in the tubular fluid becoming hyposmotic to adjacent interstitium. This can be achieved if the descending limb is permeable to water but relatively impermeable to urea and electrolytes, and the ascending limb is less permeable to water and urea than to electrolytes. In this model, a key role is played by urea which provides a driving force for water reabsorption from the descending limb. The importance of urea is illustrated in the model, firstly by simulation of a low-protein diet, and secondly by simulation of water diuresis. In both situations, reduced reabsorption of urea from the late collecting ducts causes a reduced interstitial urea concentration, which in turn causes a severe reduction in interstitial electrolyte concentration.

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