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dc.contributor.authorSchultz H.D.
dc.contributor.authorMarcus N.J.
dc.contributor.authordel Rio R.
dc.date.accessioned2020-09-02T22:28:09Z
dc.date.available2020-09-02T22:28:09Z
dc.date.issued2015
dc.identifier10.1007/978-3-319-18440-1_19
dc.identifier.citation860, , 167-185
dc.identifier.issn00652598
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6223
dc.descriptionThe treatment and management of chronic heart failure (CHF) remains an important focus for new and more effective clinical strategies. This important goal, however, is dependent upon advancing our understanding of the underlying pathophysiology. In CHF, sympathetic overactivity plays an important role in the development and progression of the cardiac and renal dysfunction and is often associated with breathing dysregulation, which in turn likely mediates or aggravates the autonomic imbalance. In this review we will summarize evidence that in CHF, the elevation in sympathetic activity and breathing instability that ultimately lead to cardiac and renal failure are driven, at least in part, by maladaptive activation of the carotid body (CB) chemoreflex. This maladaptive change derives from a tonic increase in CB afferent activity. We will focus our discussion on an understanding of mechanisms that alter CB afferent activity in CHF and its consequence on reflex control of autonomic, respiratory, renal, and cardiac function in animal models of CHF. We will also discuss the potential translational impact of targeting the CB in the treatment of CHF in humans, with relevance to other cardio-respiratory diseases. © Springer International Publishing Switzerland 2015.
dc.language.isoen
dc.publisherSpringer New York LLC
dc.subjectBlood flow
dc.subjectBreathing
dc.subjectCarotid body
dc.subjectHeart failure
dc.subjectKLF2
dc.subjectNitric oxide
dc.subjectOxidative stress
dc.subjectSympathetic nerve activity
dc.subjectangiotensin II
dc.subjectcystathionine gamma lyase
dc.subjectdipeptidyl carboxypeptidase inhibitor
dc.subjectkruppel like factor 2
dc.subjectnitric oxide
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase
dc.subjectsimvastatin
dc.subjectadrenergic stimulation
dc.subjectapnea
dc.subjectArticle
dc.subjectbreathing disorder
dc.subjectcarotid artery flow
dc.subjectcarotid body chemoreceptor
dc.subjectchemoreceptor reflex
dc.subjectchemosensitivity
dc.subjectCheyne Stokes breathing
dc.subjectexercise
dc.subjectheart failure
dc.subjectheart function
dc.subjectheart muscle blood flow
dc.subjectheart output
dc.subjectheart rate variability
dc.subjecthuman
dc.subjectkidney failure
dc.subjectkidney function
dc.subjectlung hemodynamics
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectoxygen therapy
dc.subjectpriority journal
dc.subjectprotein function
dc.subjectrespiratory sympathetic coupling
dc.subjectsensory nerve
dc.subjectsympathetic nerve
dc.subjectsympathetic tone
dc.subjectanimal
dc.subjectautonomic nervous system
dc.subjectbreathing
dc.subjectcarotid body
dc.subjectheart failure
dc.subjectheart ventricle remodeling
dc.subjecthemodynamics
dc.subjectkidney
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectreflex
dc.subjectAnimalia
dc.subjectAnimals
dc.subjectAutonomic Nervous System
dc.subjectCarotid Body
dc.subjectHeart Failure
dc.subjectHemodynamics
dc.subjectKidney
dc.subjectReflex
dc.subjectRespiration
dc.subjectVentricular Remodeling
dc.titleRole of the Carotid Body Chemoreflex in the Pathophysiology of Heart Failure: A Perspective from Animal Studies
dc.typeArticle


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