History of the urinary concentrating mechanism

Abstract

Although the processes that generate the osmotic gradients in the inner medulla remain controversial, the countercurrent mechanism for the osmotic concentration and dilution of urine is now generally accepted. It was not always so. The mechanism for urinary dilution posed no conceptual difficulties for renal physiologists. Active transport of sodium chloride by a nephron segment whose epithelium had restricted water permeability in the absence of antidiuretic hormone (ADH), presumably located in the 'distal' portion of the uriniferous tubule, was logical and based on proven and analogous processes. It was also obvious that when its water permeability was increased by ADH, water transport would be closely coupled to solute transport and reabsorbate and tubular fluid would be isosmotic. It appeared necessary to postulate the active transport of water as the final step in the production of urine which was hyperosmotic to the body fluids. Despite the fact that there was no proven example of active water transport in the animal kingdom, active water transport by the cells of the collecting ducts was proposed and was generally accepted. The simple biological solution of establishing by solute transport a hypertonic environment in an anatomically restricted portion of the kidney such that all water transport could be postulated as passive was not obvious and was scorned when proposed.