A main vector of the effects of stress is secretion of corticotrophin relea
sing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Syste
mic administration of ACTH (2.8 mu g/day sc) for 7 days in BALB/c mice caus
ed a very large increase of voluntary intake of 0.3 M NaC1 equivalent to tu
rnover of total body sodium content each day. Intracerebroventricular infus
ion of ACTH (20 ng/ day) had no effect. Intracerebroventricular infusion of
ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The la
rge sodium appetite-stimulating effect of systemic ACTH was not influenced
by concurrent systemic infusion of captopril (2 mg/day). Induction of stres
s by immobilization of mice on a running wheel caused an increase in Na app
etite associated with a 50% decrease of thymus weight, indicative of cortic
osteroid effects. The present data suggest that stress and the hormone casc
ade initiated by stress evoke a large sodium appetite in mice, which may be
an important survival mechanism in environmental conditions causing stress
.