Salt appetite is enhanced by one prior episode of sodium depletion in the rat.

A single sodium depletion enhances the salt appetite that is expressed after a second and subsequent sodium depletions. The enhanced salt intake, as measured by a decrease in latency to drink and an increase in volume of 3% NaCl ingested, is not accounted for by an increased sodium loss. The enhanced salt intake occurs even when the interval between first and second depletion is as long as 4 months. The enhanced salt appetite does not depend on the drinking of salt after the animal's first sodium depletion and is specific for NaCl but not for KCl. Moreover, it can be produced without sodium depletion by the actions of the hormones aldosterone and angiotensin on the brain. These results suggest that angiotensin and aldosterone, which are released in response to sodium depletion, (a) increase renal sodium conservation, (b) evoke a salt appetite to restore the lost sodium, and (c) produce enduring changes in the brain that prepare it for more rapid and more vigorous expression of salt appetite in response to future sodium depletions. Thus the neural mechanisms that govern salt appetite are not only activated by the hormones of sodium conservation but appear also to be organized by them for a lifelong increase in avidity for salty substances.