AJP - Regulatory, Integrative and Comparative Physiology, Vol 248, Issue 1 1-11, Copyright © 1985 by American Physiological Society
Role of renin-angiotensin-aldosterone system in NaCl appetite of rats
M. J. Fregly and N. E. Rowland
A variety of experimental paradigms is now known to induce an appetite for
NaCl solutions in rats. These include 1) bilateral adrenalectomy; 2)
hypothyroidism; 3) salivariectomy; and 4) administration of
hydrochlorothiazide, metyrapone, estrogen, methylxanthines, captopril,
propranolol, large doses of deoxycorticosterone acetate, and
intraperitoneal isotonic glucose or subcutaneous polyethylene glycol. A
point of commonality among these is that a reduction in preference
threshold accompanies the appetite for NaCl in all cases thus far tested.
An additional point is the fact that each paradigm inducing a salt
appetite, except salivariectomy, can be linked to an effect on the
renin-angiotensin-aldosterone system. The level of angiotensin II in the
brain may play a role in the induction of a salt appetite in the rat. It is
clear, however, that modest doses of mineralocorticoid hormones, given in
conjunction with the stimulus producing the salt appetite (e.g.,
adrenalectomy, thyroidectomy, or treatment with captopril), reduces NaCl
intake to control level. Although this effect can be partially explained in
most cases by the consequent reduction in angiotensin II production, the
salt appetite that occurs when mineralocorticoid concentration in blood is
high and angiotensin II concentration is low, or when both are low,
requires another explanation. This may be related to the effect of
mineralocorticoid hormones on salivary sodium concentration. The role of
the concentration of sodium in saliva on intake of NaCl solution provides
an alternative explanation for the induction of a salt appetite in rats and
merits additional study.
