Reactive oxygen species are the cause of the enhanced cardiorespiratory response induced by intermittent hypoxia in conscious rats

Terry B J Kuo, Zung Fan Yuan, You Shuei Lin, Yi Ning Lin, Weng Shan Li, Cheryl C H Yang, Ching Jung Lai

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

This study was carried out to investigate the role of reactive oxygen species (ROS) in the elevation of cardiorespiratory responses during the development of intermittent hypoxia (IH)-induced hypertension. Rats were exposed to either 30 days of IH [(30s N2)+(45s room air (RA)] or RA for 6h/day. After 5 days of exposure, stable mean arterial pressure, normalized low-frequency power of pulses interval spectrogram (a marker of cardiac sympathetic outflow), and minute ventilation (an index for arterial chemoreflex activation) were significantly increased throughout the observation period in IH-exposed rats, but not in RA-exposed rats. FosB expression in rostral ventrolateral medulla was elevated after IH exposure for 5 days. Intraperitoneal injection of MnTMPyP (a superoxide scavenger) or N-acetylcysteine (an antioxidant) prevented IH-induced elevation of the cardiorespiratory responses and lipid peroxidation of lung tissues. These results suggest that ROS are essential for IH-induced elevation of arterial chemoreflex activation and sympathetic outflow, which may, in turn, contribute to IH-induced hypertension.

Original languageEnglish
Pages (from-to)70-79
Number of pages10
JournalRespiratory Physiology and Neurobiology
Volume175
Issue number1
DOIs
Publication statusPublished - Jan 31 2011

Keywords

  • Arterial chemoreflex
  • Hypertension
  • Intermittent hypoxia
  • Reactive oxygen species
  • Sympathetic outflow

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pulmonary and Respiratory Medicine

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