NA-K-ATPASE ALONG RAT NEPHRON AFTER SUBTOTAL NEPHRECTOMY - EFFECT OF ENALAPRIL

Tubular overwork is thought to be a promoter of the tubular hypertroph y and renal failure that occur in response to renal mass reduction. Be cause Na-K-adenosinetriphosphatase (Na-K-ATPase) is an index of tubula r work, we evaluated the effects of subtotal nephrectomy and of enalap ril therapy, which delays the evolution of renal lesions, on tubular h ypertrophy and Na-K-ATPase activity along the rat nephron. Within 6 wk , 70% reduction of renal mass engendered hypertrophy of the proximal c onvoluted tubule (PCT), thick ascending limb (TAL), and collecting duc t (CD), as well as parallel increments in Na-K-ATPase activity per mil limeter tubule length (Na-K-ATPase activity per unit surface area was not modified by subtotal nephrectomy). Chronic enalapril therapy preve nted part of the hypertrophy (but not Na-K-ATPase stimulation) of the PCT and the whole stimulation of Na-K-ATPase (but not hypertrophy) in the CD, whereas it had no effect on the TAL. Enalapril effect on Na-K- ATPase in CD might result from reduced bradykinin metabolism, as the r eduction in urinary excretion of bradykinin observed in subtotally nep hrectomized rats was prevented by enalapril therapy.