AIM: The aim of the present study was to investigate whether
reactive oxygen species (ROS) in
rostral ventrolateral medulla (RVLM) modulate
cardiac sympathetic afferent reflex (CSAR) and the enhanced CSAR response caused by
microinjection of
angiotensin II (Ang II) into the
paraventricular nucleus (PVN). METHODS: Under urethane and alpha-chloralose
anaesthesia,
renal sympathetic nerve activity (RSNA) and
mean arterial pressure (MAP) were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the RSNA response to
epicardial application of
capsaicin (1.0 nmol). RESULTS: Bilateral RVLM
microinjection of tempol (a
superoxide anion scavenger) or
polyethylene glycol-superoxide dismutase (PEG-SOD, an analogue of endogenous
superoxide dismutase)
attenuated the CSAR, but did not cause significant change in baseline RSNA and MAP.
NAD(P)H oxidase inhibitors
apocynin or phenylarsine oxide (PAO) also showed similar effects, but SOD inhibitor diethyldithio-carbamic acid (DETC) enhanced the CSAR and baseline RSNA, and increased the baseline MAP. Bilateral PVN
microinjection of Ang II (0.3 nmol) enhanced the CSAR and increased RSNA and MAP, which was inhibited by the pre-treatment with RVLM administration of tempol, PEG-SOD,
apocynin or PAO. The pre-treatment with DETC in the RVLM only showed a tendency in potentiating the CSAR response of Ang II in the PVN, but significantly potentiated the RSNA and MAP responses of Ang II. CONCLUSION: These results suggest that the
NAD(P)H oxidase-derived ROS in the RVLM modulate the CSAR. The ROS in the RVLM is necessary for the enhanced CSAR response caused by Ang II in the PVN.
