Acute peripheral administration of angiotensin II (AngII) to rats vasodilates the tail and reduces both metabolic rate and body temperature. To assess the role of the brain in these responses to AngII, a discrete lesion was aimed at the subfornical organ (SFO). Such lesions are known to abolish drinking and other responses to circulating AngII. A control group was sham-operated. Following recovery from surgery, dipsogenic responses to administration of AngII (150 micrograms/kg, SC) were tested. All lesioned rats failed to drink. One week later, the changes in colonic (TC) and tail skin (TSK) temperatures were measured following an identical injection of AngII. As reported before, control rats showed a substantial rise in in TSK (maximum rise 2.5 degrees C after 12 min). In contrast, the lesioned rats showed very little rise (0.3 degrees C) in TSK, significantly less than controls. The maximal drop in TC of the control group was slightly more (0.3 degrees C) than that of the lesioned group (0.2 degrees C), but the difference was not significant. The rats were, next, acutely exposed to cold (5 degrees C). Control rats showed a significantly larger decrease in TSK than lesioned rats. Lesions were verified both anatomically and using the functional metric of AngII-induced Fos-like immunoreactivity (Fos-IR). AngII induced strong Fos-IR in the SFO, median preoptic nucleus (MnPO), and in the magnocellular hypothalamic regions of control rats. The lesions ablated the anterior part of the SFO and dorsal MnPO, and greatly attenuated AngII-induced Fos-IR in the magnocellular hypothalamic regions. Thus, there appears to be central (SFO/MnPO) mediation of both the increase in TSK following administration of AngII and the decrease in TSK in the cold.