The dependence of the salt appetite of the rat on the hormonal consequences of sodium deficiency.

Richter's discovery of the salt appetite that follows adrenalectomy (1936) raised the question: how does the brain appreciate the need for sodium so that it can mobilize the search for and ingestion of salty substances? It remains unanswered. Recent work suggests that the answer may come from an understanding of the behavioral effects of the hormones of sodium conservation. Fluharty and I have found (Behavioral Neuroscience, 1983) that treatment of salt replete rats with low doses of both angiotensin (Ang II) and a mineralocorticoid (DOCA) evokes a rapid, reliable, and specific appetite for sodium solutions, and we have proposed that the hormones of renal sodium conservation are also the hormones for the behavioral defense against sodium deficiency. We can now report: That the same combined endocrine treatment will compel rats that do not need salt to search for it in a runway. That is, sodium replete rats that have been primed for 3 days with DOCA (500 micrograms/day), which does not produce an appetite for salt, and are then given a pulse intracerebroventricular (ICV) injection of Ang II (60 ng), which by itself does not produce an appetite for salt, will run in an alleyway in order to ingest small drops of 3% NaCl. The hormones act together to make the rat avid for salt and their action is sufficient to drive it to seek salt at a distance and to ingest it at a concentration that untreated rats avoid.(ABSTRACT TRUNCATED AT 250 WORDS)