Intracerebroventricular losartan inhibits post-prandial drinking in
sheep.
Mathai, M., M. D. Evered, and M. J. McKinley.
Howard Florey Institute of Experimental Physiology and Medicine,
University of Melbourne, Parkville, Victoria, 3052, Australia and
Department of Physiology, University of Saskatchewan, Saskatoon,
Saskatchewan, S7N 5E5, Canada
APStracts 3:0322R, 1996.
We investigated the contribution of brain angiotensinergic mechanisms
to post-prandial drinking in sheep. Sheep in fluid balance were given
0.8 kg chaff for 30 min and water intake was measured for the next h.
Intracerebroventricular (ICV) infusion of the AT-1 type angiotensin
II receptor blocker losartan (1 mg/h) reduced post-prandial drinking
by about 70% (n=7, P&LT0.01) but did not affect food intake. The
same losartan dose given IV had little or no effect on prandial
drinking. Feeding increased Na+ concentrations in plasma and
cerebrospinal fluid (CSF; n=5, P&LT0.05)). ICV losartan (1 mg/h)
inhibited the drinking responses to intracarotid infusion of Ang II
(0.8 ug/min for 30 min, n=4, P&LT0.01) and to ICV infusion of 0.5
M NaCl (1 ml/h for 1 h, n=5, P&LT0.05) but had no effect on
drinking to IV infusion of 4 M NaCl (1.3 ml/min for 30 min). These
findings indicate that a brain Ang II-dependent mechanism is involved
in post-prandial drinking in sheep. They suggest also that the
mechanism by which increasing CSF Na+ causes thirst involves brain
Ang II and is different from the mechanism subserving the drinking
response to changes in blood Na+.
Received 5 July 1995; accepted in final form 26 August 1996.
APS Manuscript Number R421-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996