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Role of Endothelin‐1 in altered carotid body function by chronic intermittent hypoxia
Author(s) -
Peng YingJie,
Nanduri Jayasri,
Raghuraman Gayatri,
Wang Ning,
Kumar Ganesh K,
Prabhakar Nanduri R
Publication year - 2013
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.27.1_supplement.938.11
Subject(s) - carotid body , hypoxia (environmental) , endocrinology , endothelin receptor , medicine , endothelin 1 , intermittent hypoxia , receptor , antagonist , chemistry , carotid arteries , obstructive sleep apnea , oxygen , organic chemistry
Previous studies suggest that endothelin 1 (ET‐1) mediates the chronic intermittent hypoxia (CIH)‐evoked augmented carotid body sensitivity to hypoxia. In addition to affecting the hypoxic sensitivity, CIH induces sensory long‐term facilitation (sLTF) of the carotid body. In the present study, we examined whether ET‐1 contributes to CIH‐induced sLTF. Experiments were performed on adult male rats exposed to 10 days of normoxia or CIH (15s 5%O 2 separated by 5 min 21%O 2 , 8hrs/d). CIH increased ET‐1 content, ET‐1‐like immonustaining and ET A mRNA expression and facilitated hypoxia‐evoked ET‐1 release from the carotid body. ET A receptor antagonist BQ‐610 blocked the augmented hypoxic sensitivity but not the sLTF in CIH exposed rats. Repetitive application of ET‐1 ( 50nM) stimulated the carotid body activity but did not elicit sLTF. These results demonstrate that CIH up regulates ET‐1 in the carotid body and it contributes to CIH‐evoked augmented hypoxic sensitivity but not to sLTF. Supported by NIH‐HL‐76537, and HL‐90554.