Reactive oxygen species in rostral ventrolateral medulla modulate cardiac sympathetic afferent reflex in rats.
OBJECTIVE
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.


CONCLUSIONS
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.
Zhong
M-K
MK
Department of Physiology, Nanjing Medical University, China.
Gao
J
J
Zhang
F
F
Xu
B
B
Fan
Z-D
ZD
Wang
W
W
Zhu
G-Q
GQ
D000098:Acetophenones / Q000494:pharmacology; D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017776:Autonomic Pathways / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002211:Capsaicin / Q000494:pharmacology; D003497:Cyclic N-Oxides / Q000494:pharmacology; D016166:Free Radical Scavengers / Q000494:pharmacology; D006321:Heart / Q000294:innervation*; D007668:Kidney / Q000294:innervation; D008297:Male; D008526:Medulla Oblongata / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects; D011092:Polyethylene Glycols / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D018689:Sensory System Agents / Q000494:pharmacology; D013113:Spin Labels; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
D000098:Acetophenones; D000975:Antioxidants; D003497:Cyclic N-Oxides; D016166:Free Radical Scavengers; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D018689:Sensory System Agents; D013113:Spin Labels; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D011092:Polyethylene Glycols; C056165:acetovanillone; D013482:Superoxide Dismutase; C063471:polyethylene glycol-superoxide dismutase; D019255:NADPH Oxidases; D002211:Capsaicin; C001803:tempol