Reactive oxygen species in paraventricular nucleus modulates cardiac sympathetic afferent reflex in rats.

Our previous studies showed that angiotensin II (Ang II) in the paraventricular nucleus (PVN) potentiated the cardiac sympathetic afferent reflex (CSAR) in rats. This study investigated whether the reactive oxygen species (ROS) in the PVN modulated the CSAR and contributed to the effect of Ang II on the CSAR in rats. Under alpha-chloralose and urethane anesthesia, renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the RSNA response to epicardial application of bradykinin (0.04 and 0.4 microCompared with microinjection of saline into the PVN, superoxide anion scavenger, either tempol (20 nmol) or tiron (10 nmol), significantly decreased the CSAR (P < 0.05). Conversely, superoxide dismutase (SOD) inhibitor diethyldithio-carbamic acid (DETC, 10 nmol) potentiated the CSAR (P < 0.05). Microinjection of Ang II (0.3 nmol) into the PVN resulted in an enhanced CSAR (P < 0.05). The effect of Ang II on the CSAR was completely inhibited by pretreatment with either tempol or tiron (P < 0.05) but was not affected by DETC. On the other hand, either tempol or tiron decreased the RSNA (P < 0.05), but DETC increased the RSNA (P < 0.05). Ang II increased the RSNA (P < 0.05) and MAP (P < 0.05). The effect of Ang II on the RSNA and MAP was abolished by pretreatment with either tempol or tiron but was not affected by DETC. These results indicated that the ROS in the PVN modulated the CSAR and contributed to the effect of Ang II in the PVN on the CSAR.