AJP - Renal Physiology, Vol 270, Issue 6 997-1003, Copyright © 1996 by American Physiological Society
Na-K-ATPase along rat nephron after subtotal nephrectomy: effect of enalapril
F. Terzi, L. Cheval, C. Barlet-Bas, M. Younes-Ibrahim, B. Buffin-Meyer, M. Burtin, H. Beaufils, S. Marsy, J. P. Girolami, C. Kleinknecht and A. Doucet
Institut National de la Sante et de la Recherche Medicale (INSERM) U 426, Faculte Xavier Bichat, Paris, France.
Tubular overwork is thought to be a promoter of the tubular hypertrophy and
renal failure that occur in response to renal mass reduction. Because
Na-K-adenosinetriphosphatase (Na-K-ATPase) is an index of tubular work, we
evaluated the effects of subtotal nephrectomy and of enalapril therapy,
which delays the evolution of renal lesions, on tubular hypertrophy and
Na-K-ATPase activity along the rat nephron. Within 6 wk, 70% reduction of
renal mass engendered hypertrophy of the proximal convoluted tubule (PCT),
thick ascending limb (TAL), and collecting duct (CD), as well as parallel
increments in Na-K-ATPase activity per millimeter tubule length
(Na-K-ATPase activity per unit surface area was not modified by subtotal
nephrectomy). Chronic enalapril therapy prevented 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 reduction in urinary excretion of bradykinin
observed in subtotally nephrectomized rats was prevented by enalapril
therapy.
