Rats rendered hypothyroid by
treatment with
methimazole develop an exaggerated
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 availability of circulating
angiotensin I. In addition, we determined the influence of
aldosterone in hypothyroid
rats during the expression of spontaneous
sodium appetite and after
captopril treatment.
Captopril significantly increased (P<0.05) the daily intake of 1.8 percent NaCl (in ml/100 g
body weight) in hypothyroid
rats after 36 days of
methimazole administration (day 36 9.2 + or - 0.7 vs day 32 2.8 + or - 0.6 ml, on the 4th day after
captopril treatment). After the discontinuation of
captopril treatment, daily 1.8 percent NaCl intake reached values ranging from 10.0 + or - 0.9 to 13.9 ± 1.0 ml, 48 to 60 days
after treatment with
methimazole.
Aldosterone treatment significantly reduced (P<0.05) saline intake before (7.3 + or - 1.6 vs day 0, 14.4 + or - 1.3 ml) and after
captopril treatment. Our results demonstrate that, although hypothyroid
rats develop a
deficiency in the
production of all components of the
renin-angiotensin-aldosterone system, their capacity to synthesize
angiotensin II at the cerebral level is preserved. The partial reversal of daily 1.8 percent NaCl intake during
aldosterone treatment suggests that
sodium retention reduces both spontaneous and
captopril-induced
salt appetite