Abstract
It was reported that angiotensin II (Ang II) in paraventricular nucleus (PVN) potentiated the cardiac sympathetic afferent reflex (CSAR) in rats. In this study, we investigated whether the reactive oxygen species (ROS) contributed to the effect of Ang II on the CSAR in the PVN in anesthetized rats with sinoaortic denervation and cervical vagotomy. The CSAR was evaluated by the RSNA response to epicardial application of bradykinin (BK). Microinjection of Ang II (0.3 nmol) into the PVN significantly enhanced the CSAR compared with saline (+18.4±3.0% vs. +10.1±2.2%). The response was significantly attenuated by pretreatment with superoxide scavengers, tiron (10 nmol) or tempol (20 nmol), into the PVN (+18.4±3.0% vs. +4.3±1.5% in tiron group, and +18.4±3.0% vs. +2.8±2.5% in tempol group). Pretreatment with the NAD(P)H oxidase inhibitors, apocynin (1 nmol), or phenylarsine oxide (1 nmol) into the PVN also significantly inhibited the enhanced CSAR response induced by Ang II (+20.5±3.1% vs. +3.1±1.6% in apocynin group, and +20.5±3.1% vs. +5.0±1.7% in phenylarsine oxide group). Microinjection of the xanthine oxidase inhibitor allopurinol (10 nmol) into the PVN showed a weak inhibitory effect on the enhanced CSAR caused by Ang II (+20.4±2.5% vs. +10.4±2.4%). These findings suggested that the ROS in the PVN contributed to the effect of Ang II on the CSAR, and the generation of the ROS in the enhanced CSAR response caused by Ang II was primarily from the NAD(P)H oxidase, and partially from xanthine oxidase. (Supported by National Natural Science Fund in China (30470632) and NIH grants # PO-1 HL62222)
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call