Inhibition of distal tubular sodium reabsorption by angiotensin II

Abstract

Angiotensin II or norepinephrine was infused directly into the left renal artery of anesthetized dogs undergoing mannitol diuresis, and the right and left kidneys were compared for GFR (Ccr or Cin), RPF (Cpah), sodium excretion, and distal stop-flow sodium and inulin patterns. Both angiotensin and norepinephrine caused similar reductions of GFR and RPF on the left, as compared with the right, but only angiotensin prevented normal lowering of left distal stop-flow sodium concentration, even when length of occlusion was 14 min. The minimum effective dose was 6–12 mµg/kg min, and maximal differences between left and right sodium minima occurred with 50 mµg/kg min. Distal inulin patterns were not altered by angiotensin, nor were "postocclusive" inulin patterns. Clearance data demonstrated that when GFR changes were taken into account angiotensin caused a relative increase in sodium excretion compared to control or norepinephrine-infused dogs. These stop-flow and clearance data support the hypothesis that angiotensin inhibits distal sodium reabsorption by a direct tubular effect. No attempt was made to evaluate possible effects of angiotensin on proximal tubular sodium reabsorption.