Blood pressure and fluid-electrolyte balance in anf-transgenic mice
on high and low salt diets.
Veress, A. T., C. K. Chong, L. J. Field* and H. Sonnenberg.
Department of Physiology, University of Toronto, Canada, and
Krannert Institute of Cardiology, Indiana University School of
Medicine, USA
APStracts 2:0022R, 1995.
Transgenic mice overexpressing an atrial natriuretic factor fusion
gene (TTR-ANF) and their nontransgenic siblings were placed on either
high (8%) or low (<0.008%) salt diet for 14 days to determine whether
the life-long elevation of ANF in the transgenic animals compromised
their ability to maintain fluid-electrolyte balance. Steady-state
dietary intake and urinary output of sodium and chloride were not
statistically different between TTR-ANF and control groups on either
diet. By contrast, both water intake and urine volume were markedly
elevated in the TTR-ANF group on either diet. Arterial blood
pressure, measured in anesthetized mice at the end of the dietary
regimen, was significantly and similarly reduced in the TTR-ANF
compared to control groups on either diet, although high salt intake
was associated with increased pressure in both groups. Renal
excretion of fluid and electrolytes was studied in the anesthetized
mice before and after acute blood volume expansion. Although the
absolute increase in fluid and electrolyte excretion was much greater
on high, compared to low salt diet in both groups, TTR-ANF mice had
an exaggerated response relative to controls on either diet. On the
basis of these results we conclude: 1) When stimulated, renal salt
-conserving mechanisms are sufficiently powerful to overcome the
expected natriuretic effects of chronic elevation of plasma ANF;
however, the natriuretic potential of ANF can be expressed in the
short term when the counterregulatory mechanisms are inactivated. 2)
ANF exerts a chronic hypotensive effect which is independent of
changes in renal salt excretion. 3) Assuming that the increase in
water intake and excretion in the transgenic mice was due to
antagonism of vasopressin-induced water permeability in the nephron,
ANF may play a physiological role in regulation of renal water
excretion.
Received 25 July 1994; accepted in final form 22 January 1995.
APS Manuscript Number R406-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.