Defect in proximal and distal sodium transport in post-obstructive diuresis

Abstract

Defect in proximal and distal sodium transport in post-obstructive diuresis. Bilateral urinary obstruction was created in rats by tying a ligature around the bladder below the ureteral orifices. Sham-operated rats served as controls. Water intake was limited and food was withheld from both groups during and following obstruction. Release of the obstruction after 30hr was followed by a diuresis lasting 24 to 36hr. One group of rats was kept in balance cages before, during and after obstruction. After release of the obstruction, experimental animals had lower creatinine clearance and higher urine flow, Na, K and solute excretion than did sham-operated controls. Urine flow in the experimental animals exceeded water intake during the postobstructive period. A second group of rats was prepared identically and used for clearance and micropuncture measurements beginning 14hr after release of the obstruction. Plasma concentrations of K, urea and total solutes were elevated. C In was reduced and V, U Na V, U K V, U Osm V and C Osm were elevated. Na and water reabsorption were reduced in the proximal and distal nephron, distal K secretion was increased, and a marked defect in concentrating ability was present. The reduction in proximal Na reabsorption was not associated with a reduced peritubular capillary protein concentration. Tracer microinjection experiments with a third group of rats revealed abnormal permeability to mannitol and inulin. The defect in Na reabsorption is probably due to an increased backflux of Na, reducing net Na reabsorption. GFR is probably not identical to inulin or creatinine clearance in post-obstructive diuresis.