AJP - Renal Physiology, Vol 258, Issue 5 1164-F1172, Copyright © 1990 by American Physiological Society
Converting-enzyme inhibition abolishes polydipsia induced by dietary NaCl and K depletion
A. J. McKay, C. D. Poirier and L. N. Peterson
Department of Physiology, University of Ottawa, Ontario, Canada.
The present studies were designed to test the hypothesis that angiotensin
II (ANG II) mediates nonosmotic thirst in animals fed the low-NaCl K-free
diet by preventing the increased generation of ANG II using the
converting-enzyme inhibitor, enalapril. Animals were fed either a control
salt or low-NaCl K-free diet and were treated with or without enalapril.
Water intake in rats fed the low-NaCl K-free diet increased more than
twofold on day 3 and remained elevated over the 10-day period of study.
Treatment with enalapril (40 mg.kg-1.day-1) 1) prevented the striking rise
in plasma renin activity in rats fed the low-NaCl K-free diet, 2) led to
complete blockade of the pressor response to a 50-ng injection of
angiotensin I but not ANG II, 3) did not affect daily water intake in rats
consuming the control salt diet, 4) did not reduce basal water intake in
rats fed the low-NaCl K-free diet below values measured in control animals,
and 5) did not abolish water intake in response to osmotic stimulation.
However, enalapril treatment abolished the increase in water intake that
occurs in animals fed the low-NaCl K-free diet. In a double crossover study
using two groups of rats fed the low-NaCl K-free diet, enalapril prevented
increased water intake in rats initially fed the low-NaCl K-free diet and
rapidly inhibited increased water intake in rats fed the low-NaCl K-free
diet after the high water intake had been established.(ABSTRACT TRUNCATED
AT 250 WORDS)
