Several experiments tested whether the subfornical organ (SFO) is necessary for water or NaCl intake arising from angiotensin-converting enzyme (CE) blockade with captopril (CAP) in the drinking fluids (0.1 mg/ml). Peripheral CAP was given to rats acutely following 24-h water deprivation or chronically over several days, either with water alone available for drinking or with 0.3 M NaCl in choice with water. Control rats drank more water, and NaCl when it was available, during CAP treatment, whereas rats with SFO damage increased NaCl intake only. CAP decreased urinary volume (UV) and increased urinary potassium excretion (UKV) during rehydration with only water available and increased urinary sodium excretion (UNaV) with NaCl present. Regardless of CAP treatment, rats with SFO damage had increased electrolyte concentrations and excretions during rehydration with only water available and increased UK with NaCl present, compared with controls. Oral CAP did not have an aversive taste at the dose used here. We conclude that the SFO is necessary for CAP-enhanced water, but not NaCl, intake and suggest that different neurological mechanisms control ingestion of each fluid during CAP.

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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.

Angiotensin receptors in the most ventral part of the ventral median preoptic nucleus (VVMnPO) or organum vasculosum laminae terminalis appear to be important for salt appetite to angiotensin in rats. If so, then small lesions of this region should reduce salt appetite that is dependent on angiotensin. In separate experiments, the lesion greatly reduced salt appetite after treatments with chronic oral captopril or sodium depletion. On the other hand, the VVMnPO lesion actually enhanced salt appetite to deoxycorticosterone acetate. The lesion did not affect water intake to water deprivation, combined food-water deprivation, isoproterenol, or hypertonic saline, and basal plasma osmolality and sodium values were normal. These experiments suggest that VVMnPO lesions selectively affect angiotensin-induced salt appetite without producing the gross hydrational deficits that occur with larger lesions of the ventral forebrain.