Na,k-atpase along the rat nephron after subtotal nephrectomy :
effect of enalapril.
Terzi, Fabiola, Lydie Cheval, Catherine Barlet-Bas, Mauricio Younes
-Ibrahim, B[acute]en[acute]edicte Buffin-Meyer, Martine Burtin,
H[acute]el[grave]ene Beaufils, Sophie Marsy, Jean-Pierre Girolami,
Claire Kleinknecht, and Alain Doucet.
INSERM U 426, Facult[acute]e Xavier Bichat, Paris, INSERM U 388,
Institut Louis Bugnard, Toulouse, Laboratoire de Physiologie
Cellulaire, Coll[grave]ege de France, Paris
APStracts 2:0218F, 1995.
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-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
six weeks, 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.
Received 17 July 1995; accepted in final form 30 November 1995.
APS Manuscript Number F233-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95