We have previously reported that an angiotensin system in the anterior hypothalamic area (AHA) is enhanced in spontaneously hypertensive rats (SHRs) and that this enhancement is involved in hypertension in this strain. In addition, we have reported that some neurons in the AHA are tonically activated by endogenous angiotensins in rats. In this study, we examined whether activities of neurons receiving tonic angiotensinergic inputs in the AHA are enhanced in SHR as compared with those of Wistar Kyoto rats (WKY). Male 15- to 16- or 6-week-old SHR and age-matched WKY were anesthetized and artificially ventilated. Extracellular potentials were recorded from single neurons in the AHA. Pressure application of angiotensin II onto some neurons in the AHA increased their firing rate. The basal firing rate of angiotensin II-sensitive neurons was increased in both 15- to 16- and 6-week-old SHR than in age-matched WKY. The increase of unit firing by angiotenisn II was enhanced in both 15- to 16- and 6-week-old SHR as compared with age-matched WKY. Pressure application of losartan, an angiotensin type 1 (AT1) receptor antagonist, alone decreased the basal firing rate of angiotensin II-sensitive neurons in 15- to 16-week-old SHR and WKY. The decrease of unit firing by losartan was also enhanced in SHR as compared with WKY. Pressure application of glutamate onto angiotensin II-sensitive neurons increased their firing rate and the increase of unit firing by glutamate was enhanced in 15- to 16-week-old SHR as compared with age-matched WKY. These findings suggest that activities of angiotensin II-sensitive neurons in the AHA are enhanced in SHR as compared with WKY. It is possible that the enhanced activity of angiotensin II-sensitive neurons in the AHA of SHR is partly due to enhanced neuronal reactivity to angiotensin II.