The aim of this study was to determine whether reactive oxygen species (ROS) in the paraventricular nucleus (PVN) mediate both the cardiac sympathetic afferent reflex (CSAR) and angiotensin II-induced CSAR enhancement in chronic heart failure (CHF) rats. CSAR was evaluated from the responses of renal sympathetic nerve activity (RSNA) to epicardial application of bradykinin. In both CHF and sham-operated rats, PVN microinjection of the superoxide anion scavengers tempol or tiron almost abolished the CSAR, but the superoxide dismutase inhibitor DETC potentiated the CSAR. PVN pretreatment with tempol or tiron abolished, whereas DETC augmented, the angiotensin II-induced CSAR enhancement. In CHF rats, superoxide anion and malondialdehyde (MDA) levels in the PVN were increased, but were normalized by the AT(1) receptor antagonist losartan. PVN microinjection of tempol decreased superoxide anion and MDA levels, but epicardial application of bradykinin or PVN microinjection of angiotensin II increased superoxide anion and MDA to higher levels in CHF rats than in sham-operated rats. These results indicate that ROS in the PVN mediates the CSAR and the effect of angiotensin II in the PVN on the CSAR in both CHF and sham-operated rats. Increased ROS in the PVN are involved in the enhanced CSAR in CHF.