| Popis: |
The production of concentrated urine is achieved by osmotic equilibration of the collecting duct luminal fluid with the hypertonic medullary interstitium. The principals of countercurrent multiplication, originally proposed by Kuhn and Ryffel in 1942 [1] are now generally accepted as the mechanism by which a hypertonic medulla is created. Several studies during the 1950's established that osmolality increases from the cortex to the papillary tip in the loops of Henle, collecting ducts, and vasa recta [2–4]. Micropuncture studies during the 1960's supported the hypothesis that the single effect for countercurrent multiplication was located in the ascending limb of the loop of Henle [5, 6]. The single effect in the outer medulla, active NaCl absorption by the thick ascending limb (TAL), was established by isolated perfused tubule studies [7, 8]. The single effect in the inner medulla was less clear. Direct measurement failed to demonstrate active NaCl absorption in the thin ascending limb [5, 9]. In 1972, two studies proposed a mechanism by which countercurrent multiplication could occur in the inner medulla without active transport [10, 11]. In this review, we will discuss the “passive” mechanism and the tubular transport properties upon which this model is based, discuss recent data on urea transport and its implication for the countercurrent mechanism, and discuss potential sources of controversy and unresolved questions concerning the countercurrent system. |
