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Selective contribution of inflammation and oxidative stress to the cardiorespiratory and carotid body alterations following intermittent hypoxia
Author(s) -
Del Rio Rodrigo,
Moya Esteban A,
Iturriaga Rodrigo
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.721.1
Subject(s) - hypoxia (environmental) , intermittent hypoxia , endocrinology , oxidative stress , medicine , carotid body , hypoxic ventilatory response , nitrotyrosine , cardiorespiratory fitness , respiratory system , obstructive sleep apnea , chemistry , nitric oxide , nitric oxide synthase , organic chemistry , oxygen , stimulation
Chronic intermittent hypoxia (CIH), a main feature of obstructive sleep apnea, potentiates carotid body (CB) chemosensory and ventilatory hypoxic responses, and induces hypertension. These alterations are attributed to oxidative stress, since antioxidants prevent the enhanced chemosensory and ventilatory hypoxic responses and the hypertension. We tested if oxidative stressinduced upregulation of pro‐inflammatory cytokines TNF‐α and IL‐1β are involved in the CB and cardiorespiratory alterations during CIH. We studied the effects of ibuprofen (40 mg/Kg day) on TNF‐α, IL‐1β and 3‐nitrotyrosine (3‐NT) CB levels, chemosensory and ventilatory hypoxic responses, and blood pressure in male Sprague‐Dawley rats exposed to CIH (5%O 2 , 12 times/h for 8 h/day) for 21 days. CIH increased CB TNF‐α, IL‐1β and 3‐NT, enhanced chemosensory and ventilatory hypoxic responses, and led to hypertension. Ibuprofen prevented the increased TNF‐α and IL‐1β CB levels and cardioventilatory alterations, but not the enhanced chemosensory hypoxic response and 3‐NT accumulation. Contrarily, ascorbic acid prevented the increased CB cytokines and 3‐NT expression, the chemosensory and ventilatory potentiation, and the hypertension. Thus, present results show that CIH‐induced potentiation of CB chemosensory responses to hypoxia depends critically on the oxidative stress, but not on the increased TNF‐α and IL‐1β in the CB. Thus, we provide new evidence suggesting a plausible role for pro‐inflammatory cytokines in the control of breathing and arterial pressure during CIH acting through a CB independent pathway. Supported by FONDECYT 1100405