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Am J Physiol Regul Integr Comp Physiol 277: R1033-R1040, 1999;
0363-6119/99 $5.00
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Vol. 277, Issue 4, R1033-R1040, October 1999

Effect of adrenocorticotrophic hormone on sodium appetite in mice

D. A. Denton1, J. R. Blair-West1, M. I. McBurnie1, J. A. P. Miller2, R. S. Weisinger1, and R. M. Williams1

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


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