We examined the role of the subfornical organ (SFO) in stimulating thirst a
nd salt appetite using two procedures that initiate water and sodium ingest
ion within 1-2 h of extracellular fluid depletion. The first procedure used
injections of a diuretic (furosemide, 10 mg/kg sc) and a vasodilator (mino
xidil, 1-3 mg/kg ia) to produce hypotension concurrently with hypovolemia.
The resulting water and sodium intakes were inhibited by intravenous admini
stration of ANG II receptor antagonist (sarthran, 8 mu g.kg(-1).min(-1)) or
angiotensin-converting enzyme inhibitor (captopril, 2.5 mg/h). The second
procedure used injections of furosemide (10 mg/kg sc) and a low dose of cap
topril (5 mg/kg sc) to initiate water and sodium ingestion upon formation o
f ANG II in the brain. Electrolytic lesions of the SFO greatly reduced the
water intakes, and nearly abolished the sodium intakes, produced by these r
elatively acute treatments. These results contrast with earlier findings sh
owing little effect of SFO lesions on sodium ingestion after longer-term ex
tracellular fluid depletion.