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

Ying Han, Ying Zhang, Han Jun Wang, Xing Ya Gao, Wei Wang, Guo Qing Zhu

Research output: Contribution to journalArticle

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Abstract

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 α-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 μg). Compared 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.

Original languageEnglish (US)
Pages (from-to)82-90
Number of pages9
JournalBrain Research
Volume1058
Issue number1-2
DOIs
StatePublished - Oct 5 2005

Fingerprint

Paraventricular Hypothalamic Nucleus
Reflex
Reactive Oxygen Species
Angiotensin II
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt
Kidney
Arterial Pressure
Microinjections
Chloralose
Urethane
Bradykinin
Superoxides
Superoxide Dismutase
Anesthesia
Heart Rate
tempol

Keywords

  • Angiotensin II
  • Cardiovascular reflex
  • Paraventricular nucleus
  • Reactive oxygen species
  • Sympathetic activity

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Reactive oxygen species in paraventricular nucleus modulates cardiac sympathetic afferent reflex in rats. / Han, Ying; Zhang, Ying; Wang, Han Jun; Gao, Xing Ya; Wang, Wei; Zhu, Guo Qing.

In: Brain Research, Vol. 1058, No. 1-2, 05.10.2005, p. 82-90.

Research output: Contribution to journalArticle

Han, Ying ; Zhang, Ying ; Wang, Han Jun ; Gao, Xing Ya ; Wang, Wei ; Zhu, Guo Qing. / Reactive oxygen species in paraventricular nucleus modulates cardiac sympathetic afferent reflex in rats. In: Brain Research. 2005 ; Vol. 1058, No. 1-2. pp. 82-90.
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AU - Zhu, Guo Qing

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AB - 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 α-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 μg). Compared 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.

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