The selective appetites of wild rabbits for 500 mEq⁄1 solutions of NaCl, KC1, MgClij, and CaCl2 were studied in intact and adrenalectomized rabbits during daily treatment with either 4 IU long acting ACTH, 1.0 or 2.5 mg cortisol acetate, or 2.5 mg corticosterone. The animals were individually caged and external sodium balances performed. In intact rabbits, cortisol or corticosterone produced a significant stimulation of NaCl appetite. The response to concurrent dosage of cortisol and corticosterone was less than half of that obtained with ACTH which produced a comparable alteration of blood glucocorticoid levels but a 10-fold increase in NaCl intake. CaCl2 intake was increased in intact rabbits by cortisol treatment ut not by corticosterone or ACTH. Adrenalectomized rabbits maintained on daily steroid replacement therapy of 0.1 mg deoxycorticosterone acetate and 0.75 mg cortisone acetate showed a normal pattern of electrolyte, food, and water intake. Under these conditions ACTH produced a 4-fold increase in NaCl intake. Further addition of cortisol and corticosterone to steroid replacement therapy produced an increase in NaCl intake comparable to their effect on normal rabbits. Thereupon supplementation with ACTH resulted in an increase to a level at least as great as that found in ACTH treated, normal rabbits. The effects of ACTH and glucocorticoids on NaCl appetite were synergistic. Sodium balance showed that increases in NaCl intake were not the result of the treatment initially producing a body sodium deficit, which was then corrected by increased intake. The results provide further evidence for the hypothesis that NaCl appetite may be hormonally regulated, and demonstrate that ACTH is capable of stimulating NaCl intake by a previously unsuspected non-adrenal pathway. (Endocrinology97: 793, 1975)