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dc.contributor.authorBooth, Lindsea C.
dc.contributor.authorNishi, Erika Emy [UNIFESP]
dc.contributor.authorYao, Song T.
dc.contributor.authorRamchandra, Rohit
dc.contributor.authorLambert, Gavin W.
dc.contributor.authorSchlaich, Markus P.
dc.contributor.authorMay, Clive N.
dc.date.accessioned2016-01-24T14:40:29Z
dc.date.available2016-01-24T14:40:29Z
dc.date.issued2015-05-01
dc.identifierhttp://dx.doi.org/10.1113/expphysiol.2014.079871
dc.identifier.citationExperimental Physiology. Hoboken: Wiley-Blackwell, v. 100, n. 5, p. 485-490, 2015.
dc.identifier.issn0958-0670
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/39082
dc.description.abstractWhat is the topic of this review? Does catheter-based renal denervation effectively denervate the afferent and efferent renal nerves and does reinnervation occur? What advances does it highlight? Following catheter-based renal denervation, the afferent and efferent responses to electrical stimulation were abolished, renal sympathetic nerve activity was absent, and levels of renal noradrenaline and immunohistochemistry for tyrosine hydroxylase and calcitonin gene-related peptide were significantly reduced. By 11months after renal denervation, both the functional responses and anatomical markers of afferent and efferent renal nerves had returned to normal, indicating reinnervation.Renal denervation reduces blood pressure in animals with experimental hypertension and, recently, catheter-based renal denervation was shown to cause a prolonged decrease in blood pressure in patients with resistant hypertension. the randomized, sham-controlled Symplicity HTN-3 trial failed to meet its primary efficacy end-point, but there is evidence that renal denervation was incomplete in many patients. Currently, there is little information regarding the effectiveness of catheter-based renal denervation and the extent of reinnervation. We assessed the effectiveness of renal nerve denervation with the Symplicity Flex catheter and the functional and anatomical reinnervation at 5.5 and 11months postdenervation. in anaesthetized, non-denervated sheep, there was a high level of renal sympathetic nerve activity, and electrical stimulation of the renal nerve increased blood pressure and reduced heart rate (afferent response) and caused renal vasoconstriction and reduced renal blood flow (efferent response). Immediately after renal denervation, renal sympathetic nerve activity and the responses to electrical stimulation were absent, indicating effective denervation. By 11months after denervation, renal sympathetic nerve activity was present and the responses to electrical stimulation were normal, indicating reinnervation. Anatomical measures of renal innervation by sympathetic efferent nerves (tissue noradrenaline and tyrosine hydroxylase) and afferent sensory nerves (calcitonin gene-related peptide) demonstrated large decreases at 1week postdenervation, but normal levels at 11months postdenervation. in summary, catheter-based renal denervation is effective, but reinnervation occurs. Studies of central and renal changes postdenervation are required to understand the causes of the prolonged hypotensive response to catheter-based renal denervation in human hypertension.en
dc.description.sponsorshipNational Health and Medical Research Council of Australia (NHMRC)
dc.description.sponsorshipVictorian Government's Operational Infrastructure Support Program
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipNHMRC
dc.format.extent485-490
dc.language.isoeng
dc.publisherWiley-Blackwell
dc.relation.ispartofExperimental Physiology
dc.rightsAcesso restrito
dc.titleReinnervation following catheter-based radio-frequency renal denervationen
dc.typeArtigo
dc.rights.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.contributor.institutionUniv Melbourne
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionMonash Univ
dc.description.affiliationUniv Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3010, Australia
dc.description.affiliationUniversidade Federal de São Paulo, Dept Physiol, Cardiovasc Div, São Paulo, Brazil
dc.description.affiliationMonash Univ, Baker IDI Heart & Diabet Inst, Melbourne, Vic 3004, Australia
dc.description.affiliationMonash Univ, Cent Clin Sch, Melbourne, Vic 3004, Australia
dc.description.affiliationUnifespDepartment of Physiology, Cardiovascular Division, Federal University of São Paulo, São Paulo, Brazil
dc.description.sponsorshipIDNational Health and Medical Research Council of Australia (NHMRC): 1012100
dc.description.sponsorshipIDNational Health and Medical Research Council of Australia (NHMRC): 1054619
dc.identifier.doi10.1113/expphysiol.2014.079871
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000354220800003


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