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Mechanisms of carotid body chemoreflex dysfunction during heart failure

Schultz, Harold D.; Marcus, Noah J.; Del Rio, Rodrigo

Experimental physiology. Volume 100:Issue 2 (2015, February); pp 124-129 -- Wiley Blackwell

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  • Title:
    Mechanisms of carotid body chemoreflex dysfunction during heart failure
  • Author: Schultz, Harold D.;
    Marcus, Noah J.;
    Del Rio, Rodrigo
  • Found In: Experimental physiology. Volume 100:Issue 2 (2015, February); pp 124-129
  • Journal Title: Experimental physiology
  • Subjects: Physiology, Experimental--Periodicals; Dewey: 571.0724
  • Rights: legaldeposit
  • Publication Details: Wiley Blackwell
  • Abstract: <x xml:space="preserve">Abstract</x> New Findings

    What is the topic of this review?

    Carotid body chemoreceptor activity is tonically elevated in heart failure and contributes to morbidity due to the reflex activation of sympathetic nerve activity and destabilization of breathing. The potential causes for the enhanced chemoreceptor activation in heart failure are discussed.

    What advances does it highlight?

    The role of a chronic reduction in blood flow to the carotid body due to cardiac failure and its impact on signalling pathways in the carotid body is discussed.

    Recent advances have attracted interest in the potential for carotid body (CB) ablation or desensitization as an effective strategy for clinical treatment and management of cardiorespiratory diseases, including hypertension, heart failure, diabetes mellitus, metabolic syndrome and renal failure. These disease states have in common sympathetic overactivity, which plays an important role in the development and progression of the disease and is often associated with breathing dysregulation, which in turn is likely to mediate or aggravate the autonomic imbalance. Evidence from both chronic heart failure (CHF) patients and animal models indicates that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in sympathetic activity and the development of periodic breathing associated with the disease. Although this maladaptive change is likely to derive from altered function at all levels of the reflex arc, a tonic increase in afferent activity from CB glomus cells is likely to be a main driving force. This report focuses on our understanding of mechanisms that alter CB function in CHF and their potential translational impact on treatment of CHF.


  • Identifier: ETOClsidyv8ff10c91; System Number: LDEAvdc_100025101841.0x000001; Journal ISSN: 0958-0670; 10.1113/expphysiol.2014.079517
  • Publication Date: 2015
  • Physical Description: Electronic
  • Shelfmark(s): ELD Digital store

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