Active sodium-urea counter-transport is inducible in the basolateral membrane of rat renal initial inner medullary collecting ducts

Rat inner medullary collecting ducts (IMCD(3)s) possess a luminal Na+-dependent, active urea secretory transport process, which is upregulated by water diuresis. In this study of perfused IMCDs microdissected from base (IMCD1), middle (IMCD2), or tip (IMCD3) of the inner medulla, we tested whether furosemide diuresis alters active urea transport. Rats received furosemide (10 mg/d s.c. for 3-4 d) and were compared with pair-fed control rats. Furosemide significantly decreased urine osmolality and urea clearance, and increased blood urea nitrogen, IMCD(3)s from furosemide-treated rats had significantly lower rates of active urea secretion than IMCD(3)s from control rats. IMCD(2)s showed no active urea transport in control or furosemide-treated rats. IMCD(1)s from control rats had no active urea transport, but IMCD(1)s from furosemide-treated rats expressed significant rates of active urea reabsorption. In IMCD(1)s, this active urea reabsorptive transport process was inhibited by: (i) 0.25 mM phloretin (bath); (ii) 1 mM ouabain (bath); and (iii) replacing bath Na+ with NMDG(+); it was stimulated by 10 nM bumetanide (bath). In summary, we found that furosemide decreased active urea secretion in IMCD(3)s and induced active urea reabsorption in IMCD(1)s. The new Na+-dependent, active urea reabsorptive transport process may be a basolateral Na+-urea antiporter.