This research focuses on the brain sites for the neurohormonal activation and inhibition of thirst and salt appetite. The general hypotheses being considered are that: (a) the renal renin- angiotensin system is essential for need-induced salt appetite; (b) angiotensin II (ANGII) receptors in the subfornical organ (SFO) and organum vasculosum (OVLT) mediate ANGII-induced water and salt intake, respectively; and (c) atrial natriuretic peptide (ANP) acts at the SFO to inhibit thirst but probably does not act at the OVLT to inhibit water or NaCl intake. Proposed experiments are based on these hypotheses and test certain controversies regarding relevant key observations, such as (1) whether leakage through fenestrated capillaries regenerated after lesions of SFO and OVLT account for the observed effects of ANGII on water and salt intake; (2) whether central or peripheral ANGII receptors mediate salt appetite induced by ANGII; (3) where in the brain ANP acts to inhibit salt appetite; and (4) the basis for the augmented NaCl intake induced by systemic deoxycorticosterone (DOC) in rats with OVLT lesions. Together, these studies will strengthen the concept that circulating hormones are important regulators of fluid ingestion, and that the mechanism of this control often is by a selective action on particular circumventricular organs.
