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In the mammalian kidney the final step in the formation of a concentrated urine now is recognized to be the net extraction of water from collecting tubular fluid (1-3). Available evidence indicates that sodium and urea, in addition to water, leave this segment of the nephron (3-5). The forces that drive these molecules presumably are those which drive molecules across other biological membranes. They may include the chemical, electrical, and hydrostatic pressure gradients across the collecting tubular wall and active transport mechanisms in the wall. The rate at which these molecules move is governed also by the permeability characteristics of the wall. In the intact kidney it is difficult to assess with confidence the degree to which each of these factors affects molecular movement and consequently the final concentration of the urine. Transmural gradients in vivo may change with alteration in the medullary patterns of countercurrent flow, whereas active transport mechanisms and permeability characteristics may vary in response to hormones (6). In order to control these variables, an in vitro technique has been devised for the perfusion of collecting tubules in the isolated medullary pyramid of the rodent kidney. With this technique collecting tubular permeability can be characterized in an experimental environment

An In Vitro Demonstration of Increased Collecting Tubular Permeability to Urea in the Presence of Vasopressin*