AJP - Renal Physiology, Vol 260, Issue 5 688-F694, Copyright © 1991 by American Physiological Society
Protein-induced modulation of renin secretion is mediated by prostaglandins
S. C. Kapoor and G. G. Krishna
Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140.
Dietary protein restriction inhibits glomerular prostaglandin (PG)
synthesis and lowers plasma renin activity (PRA). To investigate the role
of PG in mediating protein-induced alterations in renin secretion, male
Sprague-Dawley rats were fed isocaloric diets providing either a standard
20% protein or a low-protein (6%) diet for 3 wk. An additional group of
rats received a PG synthesis inhibitor, meclofenamate (25 mg/l), in the
drinking water along with the 20% protein diet. Both protein restriction
and meclofenamate administration significantly (P less than 0.025) lowered
glomerular PGE2 production. Compared with standard protein intake, low
protein intake lowered basal PRA (3.96 +/- 0.16 vs. 1.58 +/- 0.12
ng.ml-1.h-1, P less than 0.001), stimulated PRA (11.6 +/- 2.3 vs. 5.5 +/-
0.7 ng.ml-1.h-1, P less than 0.025), renal venous PRA (10.0 +/- 0.7 vs.
7.02 +/- 0.72 ng.ml-1.h-1, P less than 0.02), and plasma angiotensin II
(ANG II) levels (52 +/- 5 vs. 24 +/- 3 pg/ml, P less than 0.01), while
augmenting renal tissue renin content (2.36 +/- 0.21 vs. 3.56 +/- 0.30
micrograms/mg protein, P less than 0.005). Changes in plasma and renal
tissue renin on meclofenamate treatment were similar to those observed on
6% protein diet. Both protein restriction and meclofenamate administration
increased the glomerular ANG II receptor number, while the receptor
affinity was unchanged. Thus protein restriction lowers PRA by impairing
release of renin into circulation. This impairment in renin release is
mediated by PG.
