AJP - Renal Physiology, Vol 258, Issue 2 382-F387, Copyright © 1990 by American Physiological Society
NaCl modulates captopril effects on glomerular prostaglandin synthesis and glomerular filtration
M. Rathaus, E. Podjarny, A. Pomeranz and J. Bernheim
Department of Nephrology, Meir Hospital, Kfar Saba, Israel.
Captopril stimulates glomerular prostaglandin (PG) synthesis and increases
glomerular filtration rate (GFR) in Na-repleted rats, whereas, in
Na-depleted rats, it fails to stimulate PG synthesis and decreases GFR. In
the present work the influence of chronic and acute NaCl loading on PG
synthesis and renal function was studied in Na-depleted rats receiving
captopril (LNC rats). Glomerular PGE2 and 6-keto-PGF1 alpha were not
increased in LNC rats and were significantly lower than in Na-depleted rats
(LN). Na repletion, while continuing captopril, increased PG synthesis
above control levels. Addition of captopril in vitro to the incubation
medium stimulated PGE2 synthesis in glomeruli of control rats, whereas it
depressed it in LN rats. Acute loading with NaCl in LNC rats increased
inulin and PAH clearances to values significantly greater than in control
rats and similar to those of normal rats receiving captopril. Comparable
volume loading with isotonic mannitol or 3% albumin increased inulin and
PAH clearances only to control values. The specific effect of NaCl in acute
loading was prevented by cyclooxygenase inhibition and was not mediated by
increased systemic blood pressure. The results provide evidence that the
effects of captopril on glomerular PG synthesis and renal function depend
on the state of Na balance.
