SODIUM-DEPENDENT NET UREA TRANSPORT IN RAT INITIAL INNER MEDULLARY COLLECTING DUCTS

We reported that feeding rats 8% protein for 3 wk induces net urea tra nsport and morphologic changes in initial inner medullary collecting d ucts (IMCDs) which are not present in rats fed 18% protein. In this st udy, we measured net urea transport in microperfused initial IMCDs fro m rats fed 8% protein for greater than or equal to 3 wk and tested the effect of inhibiting Na+/ K+-ATPase activity and found that adding 1 mM ouabain to the bath reversibly inhibited net urea transport from 14 +/- 3 to 6 +/- 2 pmol/mm per min (P < 0.01), and that replacing potas sium (with sodium) in the bath reversibly inhibited net urea transport from 18 +/- 3 to 5 +/- 0 pmol/mm per min (P < 0.01). Replacing perfus ate sodium with N-methyl-D-glucamine reversibly inhibited net urea tra nsport from 12 +/- 2 to 0 +/- 1 pmol/mm per min (P < 0.01), whereas re placing bath sodium had no significant effect on net urea transport. A dding 10 nM vasopressin to the bath exerted no significant effect on n et urea transport. Finally, we measured Na+/K+-ATPase activity in init ial and terminal IMCDs from rats fed 18% or 8% protein and found no si gnificant difference in either subsegment. Thus, net urea transport in initial IMCDs from rats fed 8% protein for, 3 wk requires sodium in t he lumen, is reduced by inhibiting Na+/K+-ATPase, and is unchanged by vasopressin or phloretin. These results suggest that net urea transpor t may occur via a novel, secondary active, sodium-urea cotransporter.