AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 6 1071-R1077, Copyright © 1986 by American Physiological Society
Neuroendocrine factors mediating polydipsia induced by dietary Na, Cl, and K depletion
A. Saikaley, D. Bichet, J. Kucharczyk and L. N. Peterson
We investigated whether the increased intake of water during dietary
electrolyte depletion is related to activation of the renin-angiotensin
system. Young adult male rats were fed a low Na-, Cl-, K-free (low-salt)
diet for 2 wk during which measurements were made of daily water intake and
urine volume, plasma osmolality (Posm) and electrolytes, and plasma renin
activity (PRA) and angiotensin I (ANG I) concentration. Water intake and
urine output increased on day 3 of the low-salt diet, reached a maximum on
day 4, and remained elevated, paralleling the time course of increases in
PRA and ANG I plasma concentrations. Posm was normal after 2 days on the
low-salt, although it was significantly lower by day 11. Renal
concentrating ability was not different from controls after 6 days, but was
significantly reduced after 11 days of treatment. Electrolytic lesions of
the subfornical organ (SFO) abolished the low-salt diet-induced polydipsia,
but had no effect on the diet-induced increases in PRA and plasma ANG I
concentration. These data demonstrate that polydipsia induced by feeding a
low-salt diet can develop in the presence of a normal or reduced Posm and
precedes the development of a renal concentrating defect. The primary
polydipsia is associated with elevated PRA and ANG I and appears to be
mediated by angiotensin receptors in the SFO.
