Salt intake modulates the developmental expression of renal
kallikrein and bradykinin b2 receptors.
El-Dahr, Samir S., Igor V. Yosipiv, Dianne G. Muchant, and Robert L.
Chevalier.
Section of Pediatric Nephrology, Tulane University School of
Medicine, New Orleans, Louisiana, 70112, and Division of Pediatric
Nephrology, University of Virginia Health Sciences Center,
Charlottesville, Virginia 22908
APStracts 2:0177F, 1995.
The mechanisms involved in the postnatal induction of renal kallikrein
gene transcription and enzymatic activity are unknown. The present
study was designed to test the hypothesis that salt (NaCl) intake
regulates the ontogeny of renal kallikrein gene expression and
enzymatic activity and urinary kallikrein excretion. Newborn rats
were artificially fed via a gastric tube with a milk formula
containing either normal (25 mEq/L, same as in maternal milk) or high
(145 mEq/L) NaCl content from day 7 to 14 of postnatal life. High
salt feeding decreased renal kallikrein mRNA levels (p&LT0.05),
and kallikrein-like activity (p&LT0.05) compared to rat pups on
normal salt intake. However, urinary kallikrein excretion (Ukal) was
not different on chronic high vs. normal salt intake. Furthermore,
acute volume expansion (0.9% saline, 1% BW i.v.) did not alter Ukal
in either group of developing rats. In adult rats, 1% NaCl in the
drinking water for 10 days decreased renal active kallikrein contents
(p&LT0.05), but did not alter kallikrein mRNA levels compared to
pair-fed rats on normal salt diet. Acute volume expansion in adult
rats decreased active Ukal in the high salt group only (p&LT0.05).
High salt feeding upregulated bradykinin B2 receptor mRNA in the
developing rats (p&LT0.05). We conclude that chronic salt loading
suppresses the postnatal rise in renal kallikrein gene expression and
enzymatic activity, indicating that sodium intake is an important
factor in the maturation of renal kallikrein synthesis. The data also
suggest that bradykinin B2 receptor gene expression in the developing
kidney may be subject to reciprocal feedback regulation by endogenous
kallikrein-kinin activity.
Received 24 April 1995; accepted in final form 11 September 1995.
APS Manuscript Number F132-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95