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Am J Physiol Regul Integr Comp Physiol 281: R723-R729, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 3, R723-R729, September 2001

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats

G. H. M. Schoorlemmer1,2, A. K. Johnson1,2,3,4, and R. L. Thunhorst1,2

Departments of 1 Psychology, 3 Pharmacology, 4 Exercise Science, and the 2 Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242-1407

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 ± 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 ± 12% (n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10-15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.

sodium depletion; blood volume; blood pressure; sodium excretion; vasopressin


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