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)+(45 s room air (RA)] or RA for 6 h/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.
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