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VEGF up‐regulation and vascular area enlargement induced by intermittent hypoxia in the rat carotid body is not secondary to oxidative stress
Author(s) -
Iturriaga Rodrigo,
Moya Esteban A,
Rio Rodrigo Del
Publication year - 2012
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.26.1_supplement.898.1
Subject(s) - hypoxia (environmental) , endocrinology , oxidative stress , medicine , ascorbic acid , vascular endothelial growth factor , intermittent hypoxia , long term potentiation , chemistry , obstructive sleep apnea , vegf receptors , oxygen , receptor , organic chemistry , food science
Chronic intermittent hypoxia (CIH), a main feature of obstructive sleep apnea, potentiated the carotid body (CB) chemosensory responses to acute hypoxia, enlarges the vascular area and increased the VEGF expression in the CB. Since oxidative stress plays an essential role in the CIH‐induced CB chemosensory potentiation and by the fact that VEGF may be directly up‐regulated by oxidative stress, we hypothesized if the treatment with an antioxidant may impede the increased expression of VEGF and the enlarged vascular area in the CB of rats exposed to CIH. Thus, we tested the effects of ascorbic acid on the vascular area enlargement and the VEGF immunoreactivity (VEGF‐ir) in the CB of rats exposed to 5%O2, 12 times/hr for 8 hrs or sham condition for 21 days. We found that CIH increased VEGF‐ir and enlarged the vascular area in the CB by increasing the size of the blood vessels, although the number of blood vessels was unchanged. Ascorbic acid, which prevented the CB chemosensory potentiation to hypoxia failed to impede the vascular enlargement and the increased VEGF‐ir in the CB. Thus, our results suggest that CB vascular changes, including VEGF up‐regulation may result of the direct hypoxic stimulation during CIH exposure, and not secondary to the increased oxidative stress, which is involved in the potentiation of the CB chemosensory responses to hypoxia. Supported by FONDECYT 1100405