Three-hour infusions of angiotensin II (ANG II) agonists and antagonists were used to determine the relative sites of action of ANG in producing water drinking and salt appetite. In the first experiment, lateral ventricular (LV) but not fourth ventricular (4V) ANG II elicited water and saline intake, and LV but not 4V sarile, a competitive ANG II receptor blocker, reduced saline intake aroused by ip injections of 10 mg/kg furosemide and 6 mg/kg captopril. In the second experiment, water, but not saline, intake to furosemide-captopril treatment was reduced by sarile infusions into the subfornical organ (SFO). It is concluded that (a) brain ANG receptors for water and saline intakes are more accessible from the forebrain than the hindbrain ventricles and (b) receptors for water drinking, but not saline intake, after captopril reside in part in the SFO. Salt appetite appears to be dependent on ANG II receptors somewhere in the forebrain other than in the SFO.

Two experiments were designed to test whether angiotensin (ANG) synthesis or receptor activation in the ventral preoptic region is critical for ANG-induced salt appetite in rats. In Experiment 1, infusions of ANG into the subfornical organ (SFO) produced water drinking without saline intake, but infusions near the organum vasculosum laminae terminalis (OVLT) produced both water and saline drinking. Thus, forebrain areas that support water drinking to ANG do not all support salt appetite. In Experiment 2, rats were given oral captopril (CAP) to enhance daily intake of water and saline solution by increasing ANG II synthesis in the brain. CAP microinjected into the SFO reduced CAP-enhanced water drinking without affecting saline intake, but CAP in the OVLT reduced enhanced saline intake without affecting water drinking. Thus, ANG acting in the OVLT, the most ventral part of the median preoptic nucleus, or other nearby structures is important for ANG-induced salt appetite.

These experiments were conducted to test whether drinking to ip captopril or to intraventricular carbachol requires an intact fiber system from the ventral subfornical organ (SFO). Wire-knife cuts were made through the wall of the third ventricle ventral to the SFO. Control rats had either sham lesions or histologically identified missed cuts. Rats with good cuts (a) drank less than either control group after ip injections of 4 mg/kg captopril, (b) drank normal amounts of 0.3 M NaCl solution when captopril was placed in the drinking water at 0.1 mg/ml, (c) drank less water but a normal amount of saline after 6 mg/kg captopril ip and 10 mg/kg furosemide diuretic ip, and (d) drank normal amounts of water after lateral ventricular injections of 1.2 or 4 nmol of carbachol. The results of the captopril experiments confirm predictions based on studies of SFO lesions and suggest that captopril causes water, but not saline, drinking via an angiotensin-related mechanism acting at the SFO. The carbachol experiment indicates either that the SFO is not a unique receptor site for ventricular carbachol or that the fibers mediating this response do not require the pathways through the ventral pole of the SFO.

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