Preoptic angiotensin and salt appetite.
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. Salt appetite is easily elicited by prolonged sodium depletion or hypovolemia in rats. It has recently become clear that two hormones, angiotensin and aldosterone, are responsible for the generation of much of this behavior (see Rowland & Fregly, 1988, for review). For instance, a blockade of peripheral angiotensin synthesis (Moe, Weiss, & Epstein, 1984) or of central angiotensin or aldosterone receptors (Sakai, Nicolai'dis, & Epstein, 1986; Weiss, Moe, & Epstein, 1986) can specifically reduce salt appetite in sodium depleted rats; furthermore, infusions of angiotensin into the brain ventricles of either normally hydra ted (Avrith & Fitzsimons, 1980; Bryant, Epstein, Fitzsimons, & Fluharty, 1980) or sodiumdepleted rats (Fitts, Thunhorst, & Simpson, 1985) increase saline drinking. The receptors responsible for angiotensin-induced salt appetite are in the forebrain because salt appetite can be aroused or blocked by infusions of angiotensin or its blockers in the forebrain ventricles but not in the fourth ventricle (Fitts & Masson, 1989). One site in the forebrain that is rich in angiotensin receptors, the subfornical organ (SFO), appears not to be critical for salt appetite because lesions of the SFO, fiber disconnections ventral to the SFO, and infusions of angiotensin receptor blockers in the SFO do not affect salt appetite (Fitts & Masson, 1989; Masson & Fitts, 1989; Schulkin, Eng, & Miselis, 1983; Thunhorst, Fitts, & Simpson, 1987). However, these studies did not rule out the possibility that angiotensin receptors in the SFO could support a part of the salt appetite response, perhaps through a summation with the output of other receptive areas.