Effect of chronic oral administration of a low dose of captopril on sodiumappetite of hypothyroid rats. Influence of aldosterone treatment

Rats rendered hypothyroid by treatment with methimazole develop an exaggera ted sodium appetite. We investigated here the capacity of hypothyroid rats (N = 12 for each group) to respond to a low dose of captopril added to the ration, a paradigm which induces an increase in angiotensin II synthesis in cerebral areas that regulate sodium appetite by increasing the availabilit y of circulating angiotensin I. In addition, we determined the influence of aldosterone in hypothyroid rats during the expression of spontaneous sodiu m appetite and after captopril treatment. Captopril significantly increased (P<0.05) the daily intake of 1.8% NaCl (in ml/100 g body weight) in hypoth yroid rats after 36 days of methimazole administration (day 36: 9.2 <plus/m inus> 0.7 vs day 32: 2.8 +/- 0.6 mi, on the 4th day after captopril treatme nt). After the discontinuation of captopril treatment, daily 1.8% NaCl inta ke reached values ranging from 10.0 +/- 0.9 to 13.9 +/- 1.0 ml, 48 to 60 da ys after treatment with methimazole, Aldosterone treatment significantly re duced (P<0.05) saline intake before (7.3 <plus/minus> 1.6 vs day 0, 14.4 +/ - 1.3 ml) and after captopril treatment, Our results demonstrate that, alth ough hypothyroid rats develop a deficiency in the production of all compone nts of the renin-angiotensin-aldosterone system, their capacity to synthesi ze angiotensin II at the cerebral level is preserved. The partial reversal of daily 1.8% NaCl intake during aldosterone treatment suggests that sodium retention reduces both spontaneous and captopril-induced salt appetite.