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Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia.

Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Research Abstract Details 

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  • Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Abstract Text:

    nanduri r prabhakarNanduri R Prabhakar,thomas e dickThomas E Dick,jayasri nanduriJayasri Nanduri,ganesh k kumarGanesh K Kumar,

    Patients with recurrent apnoeas exhibit autonomic abnormalities manifested as persistent increase in sympathetic nerve activity (SNA). Several studies suggest that chronic intermittent hypoxia (CIH) resulting from recurrent apnoeas is a major stimulus for evoking autonomic morbidity. Although it has been proposed that CIH, by way of activating the chemoreceptor reflex, leads to sympathetic excitation, the underlying mechanisms are incompletely understood. Studies on experimental models have provided new insights into the mechanisms associated with CIH-evoked sympathoexcitation. The purpose of this article is to highlight recent information on systemic, cellular and molecular analysis of the effects of CIH on chemoreceptor-mediated sympathoexcitation. Chronic intermittent hypoxia exerts two major effects on the chemoreceptor reflex: (a) augmentation of the carotid body and sympathetic effector responses to acute hypoxia; and (b) induction of long-lasting activation of both the sensor and the effector that persists several hours after termination of CIH. Available evidence indicates that CIH may facilitate processing of chemoreceptor afferent information at the central nervous system. Recent studies suggest that reactive oxygen species-mediated signalling is a major cellular mechanism, and transcriptional activation by hypoxia-inducible factor-1 is one of the critical molecular mechanisms underlying chemoreceptor-mediated sympathoexcitation by CIH.

    Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Publishing Authors By Initials

    nr prabhakarNR Prabhakar,te dickTE Dick,j nanduriJ Nanduri,gk kumarGK Kumar,

    For similar nervous system: peripheral nervous system: autonomic nervous system: sympathetic nervous system research abstracts see: nervous system: peripheral nervous system: autonomic nervous system: sympathetic nervous system research

    PUBMED ID PMID:

    MEDLINE DATE:

    Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Journal Published:

    PUBLICATION TYPE: Review

    Journal: Experimental physiology

    VOLUME: 92

    Page Numbers: 39-44

    Journal Abbreviation: Exp. Physiol.

    ISSN: 0958-0670

    DAY: 23

    MONTH: 11

    YEAR: 2006

    Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Information

    Number of References: 49

    LANGUAGE: eng

    NlmUniqueID: 9002940

    Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Keywords Mesh Terms:

    KEYWORDS: Sympathetic Nervous System

    MESH TERMS: physiopathology

    Chemical & Substance for Abstract: Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia. Information

    Substance Name: Reactive Oxygen Species

    Registry Number: 0

    Grant and Affiliation Information for Systemic, cellular and molecular analysis of chemoreflex-mediated sympathoexcitation by chronic intermittent hypoxia.

    AFFILIATION: Department of Physiology & Biophysics, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44109, USA. nrp@case.edu. nrp@case.edu

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NHLBI

    GRANT: HL-46462

    ACRONYM: HL

    MEDLINETA: Exp Physiol

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    Number Hits: 0

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