The Influence of Vasopressin on the Permeability of the Mammalian Collecting Duct to Urea*

The efficient operation of the renal concentrating mechanism is dependent tipon the action of vasopressin on the permeability of the distal convoluted tubule to water (1). In the presence of this hormone, hypotonic fluid entering the distal convolution equilibrates osmotically with fluid in the surrounding renal cortical tissue, and isotonicity of the fluid delivered to the collecting ducts is achieved (1, 2). The collecting ducts are surrounded by a medullary interstitium which is variably hyperosmolal to plasma (3-5). The osmotic movement of water from collecting duct lumen to medullary interstitium results in the excretion of a hypertonic urine. Despite evidence that movement of water across the collecting duct epithelium may occur in the apparent absence of vasopressin (6, 7), most schemes of the urinary concentrating process include the hypothesis that water permeability in this segment of the nephron is enhanced by this hormone. The present study was designed to test that hypothesis. Kinetic analysis of the action of vasopressin on the movement of water and solute across the toad skin indicates that the hormone acts to increase the pore size in this epithelial membrane (8, 9). If vasopressin exerts a similar action on the collecting duct epithelium, the permeability of the membrane to various partially permeant solutes should be affected by this agent. Since the urea concentration within the collecting duct fluid rises as water is abstracted from the lumen (10) it may be concluded that this membrane offers a barrier to the free diffusion of this molecule. It was therefore anticipated that an effect of vasopressin on the permeability of the collecting duct epithelial