| Differential expression of pro-inflammatory cytokines, endothelin-1 and nitric oxide synthases in the rat carotid body exposed to intermittent hypoxia. | |
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MedLine Citation:
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PMID: 21555119 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The enhanced carotid body (CB) chemosensory response to hypoxia induced by chronic intermittent hypoxia (CIH) has been attributed to oxidative stress, which is expected to increase the expression of chemosensory modulators including chemoexcitatory pro-inflammatory cytokines in the CB. Accordingly, we studied the time-course of the changes in the immunohistological expression of TNF-α, IL-1β, IL-6, ET-1, iNOS, eNOS and 3-nitrotyrosine in the CB, along with the progression of enhanced CB chemosensory responses to acute hypoxia in male Sprague-Dawley rats exposed to CIH (5%O(2), 12times/h per 8h) for 7, 14 and 21days. Exposure to CIH for 7days resulted in a sustained potentiation of CB chemosensory responses to acute hypoxia, which persisted until 21days of CIH. The chemosensory potentiation was paralleled by an increased 3-nitrotyrosine expression in the CB. On the contrary, CIH produced a transient 2-fold increase of ET-1 immunoreactivity at 7days, a decrease in eNOS immunoreactivity, and a delayed but progressive increase of TNF-α, IL-1β and iNOS immunoreactivity, which was not associated with changes in systemic plasma levels or immune cell invasion within the CB. Thus, present results suggest that the local expression of chemosensory modulators and pro-inflammatory cytokines in the CB may have different temporal contribution to the CB chemosensory potentiation induced by CIH. |
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Authors:
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Rodrigo Del Rio; Esteban A Moya; Rodrigo Iturriaga |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-4-21 |
Journal Detail:
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Title: Brain research Volume: - ISSN: 1872-6240 ISO Abbreviation: - Publication Date: 2011 Apr |
Date Detail:
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Created Date: 2011-5-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0045503 Medline TA: Brain Res Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 Elsevier B.V. All rights reserved. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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