Sodium chloride injections in the brain induce natriuresis and
blood pressure responses sensitive to angiotensin ii at-1
receptors.
Rohmeiss, Peter, Christian Beyer, Eleonore Nagy, Carsten
Tsch[diaeresis]ope, Susanne H[diaeresis]ohle, Manfred Strauch, and
Thomas Unger.
Department of Pharmacology, University of Kiel and Department of
Nephrology, Klinikum Mannheim*, University of Heidelberg, Germany
APStracts 2:0095F, 1995.
In the present study we tested the hypothesis that the natriuretic and
pressor effects of intracerebroventriculary (i.c.v.) injected
hypertonic saline involve a central angiotensinergic pathway. All
experiments were performed in conscious Wistar rats. Bolus i.c.v.
injections of hypertonic saline (0.19, 0.23, 0.30, 0.60 M; injection
volume 5 l) induced a concentration-dependent increase of renal
sodium excretion without affecting urinary flow. The increase in
renal sodium excretion after the two highest saline concentrations
was accompanied by significant increases in mean arterial blood
pressure. Pretreatment with the angiotensin AT-1 receptor antagonist,
losartan (5 g i.c.v.), reduced the natriuretic effect of 0.23 M and
0.30 M saline but did not affect the natriuresis induced by 0.60 M
saline. The increase in mean arterial blood pressure after 0.30 M and
0.60 M saline i.c.v. was markedly attenuated by i.c.v. pretreatment
with losartan. Our results demonstrate the involvement of a central
angiotensinergic mechanism in the natriuretic and pressor responses
to hypertonic saline. Beside the ANG II-mediated natriuresis, an
additional natriuretic mechanism - independent of ANG II and
associated with the saline-induced pressor effect - seems to be
recruited with increasing concentrations of saline in the
cerebrospinal fluid.
Received 21 December 1993; accepted in final form 16 May 1995.
APS Manuscript Number F455-3.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.