Jeff M. Sands, M.D.
Professor of Medicine
Emory University, Renal Division
WMRB Room 338, 1639 Pierce Drive, NE
Atlanta, GA 30322
Urea transport in the renal inner medulla is important for the conservation of body water due to its role in the urine concentrating mechanism. Urea is transported by facilitated and by active urea transporter processes. The vasopressin-regulated facilitated urea transporter (UT-A1) in the terminal inner medullary collecting duct (IMCD) permits very high rates of transepithelial urea transport and results in the delivery of large amounts of urea into the deepest portions of the inner medulla where it is needed to maintain a high interstitial osmolality for concentrating the urine maximally. Surprisingly, UT-A1 is up-regulated when urinary concentrating ability is reduced. In addition to the UT-A family, 3 secondary active, sodium-dependent urea transport processes have been functionally characterized in IMCD subsegments:  active urea absorption in the apical membrane of initial IMCDs from hypercalcemic rats or rats fed a low-protein diet;  active urea absorption in the basolateral membrane of initial IMCDs from furosemide-treated rats; and  active urea secretion in the apical membrane of terminal IMCDs from untreated rats. The response of these active urea transporters to reductions in urine concentrating ability follows 2 paradigms: one occurs with hypercalcemia, furosemide treatment, or a low-protein diet while the second occurs only in water diuresis. In the first paradigm, active urea secretion decreases in IMCD3s, active urea reabsorption appears in IMCD1s, and no active urea transport is detectable in IMCD2s. In the second pattern, active urea secretion is up-regulated in IMCD3s and appears in IMCD2s.1998-1999 Mathematics in Biology
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