Effect of adrenocorticotrophic hormone on sodium appetite in mice

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1999-10, Vol.277 (4), p.1033-R1040
• Main Authors: Denton, D. A, Blair-West, J. R, McBurnie, M. I, Miller, J. A. P, Weisinger, R. S, Williams, R. M
• Format: Article
• Language: English
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.1999.277.4.R1033

1  Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052; and 2  The Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria, Australia 3052 A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 µg/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion 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 large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress. corticotrophin releasing factor; captopril; immobilization; stress; sodium intake; water intake