This study examined the influence of oestrogen on cardiovascular responses to hypotension produced by administration of isoproterenol (Isop) and on neural activation in hindbrain nuclei mediating these responses. We first measured mean arterial pressure (MAP) and heart rate (HR) after administration of isoproterenol, a beta-adrenergic agonist that increases circulating levels of AngII, in ovariectomized (OVX) rats treated with oestradiol benzoate (EB). We then evaluated EB effects on Isop-induced Fos immunoreactivity (Fos-IR) in the hindbrain baroreflex circuit. To control for weight loss associated with oestrogen replacement in OVX rats, we food restricted a separate group of OVX rats and evaluated Isop-induced changes in MAP, HR and Fos-IR. The depressor response to Isop was significantly attenuated by EB, which also produced a disproportionate increase in HR. These effects were not secondary to loss of body weight after EB treatment, because cardiovascular responses to Isop in food restricted rats were similar to those in OVX rats treated with the oil vehicle. Isop significantly increased Fos-IR in the nucleus of the solitary tract (NTS), area postrema (AP), rostral ventrolateral medulla (RVLM), and lateral parabrachial nucleus (lPBN); however, EB significantly attenuated the increase in the AP and in the lPBN. Again, these effects were not secondary to body weight loss, because food restricted rats had the same pattern of Fos-IR as did rats treated with the oil vehicle. These results suggest that EB modifies cardiovascular responses to Isop, possibly by decreasing activation of the AP and lPBN.