Endogenous angiotensin ii inhibits natriuresis following acute
volume expansion in the neonatal rat.
Chevalier, Robert L, Barbara A. Thornhill, David C. Belmonte, Alex J.
Baertschi.
Department of Pediatrics, Department of Physiology, University of
Virginia, Charlottesville, Virginia
APStracts 2:0252R, 1995.
Compared to the adult, the neonatal renal natriuretic response to
acute volume expansion (VE) is attenuated. To test the hypothesis
that antinatriuresis is mediated by endogenous angiotensin II (AII),
Sprague-Dawley rats were given losartan, an AII AT1-type receptor
inhibitor, 40 mg/kg/day, from birth to 14-17 d. Control littermates
received saline vehicle. Anesthetized rats underwent acute saline VE
for measurement of mean arterial blood pressure (MAP), plasma
aldosterone concentration (Paldo), plasma atrial natriuretic peptide
(PANP), glomerular filtration rate (GFR), sodium excretion (UNaV),
potassium excretion (UKV) and urine cyclic GMP excretion (UcGMPV).
Losartan increased basal urine flow five-fold, UNaV ten-fold, and UKV
twofold. Acute VE induced marked diuresis, natriuresis and kaliuresis
in the losartan, but not the saline group. This occurred without
change in Paldo, PANP, and despite lower MAP, GFR, and UcGMPV. In
addition, losartan did not affect release of cGMP from isolated
glomeruli stimulated by ANP or sodium nitroprusside. We conclude that
the limited renal response to acute VE in the neonate results from
stimulation of tubular Na reabsorption by AII acting on the ATI
receptor.
Received 24 May 1995; accepted in final form 29 August 1995.
APS Manuscript Number R316-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.