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Intermittent Hypoxia Attenuates Carotid Baro‐Receptor Activity via Endothelin‐1
Author(s) -
Peng YingJie,
Nanduri Jayasri,
Kumar Ganesh,
Prabhakar Nanduri
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.669.10
Previous studies reported that sleep‐apnea patients and rodents exposed to chronic intermittent hypoxia (CIH) exhibit attenuated baro‐reflex function. In the present study we investigated the effects of chronic IH on carotid baroreceptor activity and assessed the underlying mechanism(s). Experiments were performed on adult male rats exposed to two weeks of normoxia or chronic IH (15s 5%O 2 followed by 5 min 21%O 2 , 8hrs/d). Carotid baroreceptor activity was recorded from an ex vivo carotid sinus preparation. In response to increased carotid sinus pressure baroreceptor activity increased in control preparations and this response was markedly attenuated in chronic IH treated preparations. Chronic IH increased endothelin‐1 (ET‐1) content and endothelin converting enzyme (ECE) activity in the sinus region. Chronic IH‐induced attenuation of baroreceptor response was prevented by ET A but not ET B receptor antagonist. Reactive oxygen species (ROS) levels were elevated in IH‐treated sinus region and ROS scavenger prevented the enhanced ECE activity, ET‐1 expression, and restored baro‐receptor responses in chronic IH treated rats. These observations demonstrate that chronic IH down‐regulates carotid baroreceptor function via up‐regulation of ET‐1 involving ECE activation in the carotid sinus region. Supported by NIH ‐HL‐76537, and HL‐90554.