Sympathetic overactivity occurs before hypertension in the two-kidney, one-clip model
dc.contributor.author | Oliveira-Sales, Elizabeth Barbosa de [UNIFESP] | |
dc.contributor.author | Colombari, Eduardo | |
dc.contributor.author | Abdala, Ana Paula Lima [UNIFESP] | |
dc.contributor.author | Campos, Ruy Ribeiro [UNIFESP] | |
dc.contributor.author | Paton, Julian Francis Richmond | |
dc.date.accessioned | 2019-01-21T10:30:15Z | |
dc.date.available | 2019-01-21T10:30:15Z | |
dc.date.issued | 2016 | |
dc.description.abstract | Our knowledge of mechanisms responsible for both the development and the maintenance of hypertension remains incomplete in the Goldblatt (two-kidney, one-clip | en |
dc.description.abstract | 2K1C) model. We tested the hypothesis that elevated sympathetic nerve activity (SNA) occurs before the onset of hypertension in 2K1C rats, considering the time course of the increase in SNA in relationship to the onset of the hypertension. We used a decorticated in situ working heart-brainstem preparation of three groups of male Wistar rats, namely sham-operated animals (SHAM, n = 7) and animals 3 weeks post-2K1C, of which some were hypertensive (2K1C-H, n = 6) and others normotensive (2K1C-N, n = 9), as determined in vivo a priori. Perfusion pressure was higher in both 2K1C groups (2K1C-H, 76 +/- 1 mmHg | en |
dc.description.abstract | 2K1C-N, 74 +/- 3 mmHg | en |
dc.description.abstract | versus SHAM, 60 +/- 2 mmHg, P < 0.05). The SNA was significantly elevated in both 2K1C groups (2K1C-H, 47.7 +/- 6.1 mu V | en |
dc.description.abstract | 2K1C-N, 32.8 +/- 2.8 mu V | en |
dc.description.abstract | versus SHAM, 20.5 +/- 2.5 mu V, P < 0.05) owing to its increased respiratory modulation | en |
dc.description.abstract | the chemoreflex was augmented and baroreflex depressed. Precollicular transection reduced SNA in all groups (2K1C-H, -32.5 +/- 7.5% | en |
dc.description.abstract | 2K1C-NH, -48 +/- 6.9% | en |
dc.description.abstract | versus SHAM, -13.2 +/- 1%, P < 0.05). Subsequent medullary spinal cord transection abolished SNA in both SHAM and 2K1C-N groups, but decreased it by only 57 +/- 5.5% in 2K1C-H preparations. Thus, SNA is raised before the onset of hypertension, by the third week after renal artery clipping, and this originates, in part, from its enhanced respiratory modulation. Spinal circuits contribute to the elevation of SNA in the 2K1C model, but only after hypertension has developed. | en |
dc.description.affiliation | School of Physiology & Pharmacology, Bristol Heart Institute, University of Bristol, Bristol, UK | |
dc.description.affiliation | Department of Physiology, Federal University of Sao Paulo, UNIFESP, SP, Brazil | |
dc.description.affiliation | Department of Physiology & Pathology, School of Dentistry of Araraquara, São Paulo State University, UNESP, Araraquara, SP, Brazil | |
dc.description.affiliationUnifesp | Department of Physiology, Federal University of Sao Paulo, UNIFESP, SP, Brazil | |
dc.description.source | Web of Science | |
dc.description.sponsorship | Coordenacao de Aperfeicoamento de pessoal de Nivel Superior (CAPES, Brazil) [3496/07-4] | |
dc.description.sponsorship | British Heart Foundation [RG/12/6/29670] | |
dc.description.sponsorship | National Institutes of Health [RO1 NS069220] | |
dc.description.sponsorship | Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) | |
dc.description.sponsorship | Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) from Brazil | |
dc.description.sponsorship | Benjamin Meaker Fellowship from the University of Bristol | |
dc.description.sponsorship | Royal Society Wolfson Research Merit Award | |
dc.description.sponsorshipID | CAPES: 3496/07-4 | |
dc.description.sponsorshipID | British Heart Foundation: RG/12/6/29670 | |
dc.description.sponsorshipID | National Institutes of Health: RO1 NS069220 | |
dc.format.extent | 67-80 | |
dc.identifier | https://doi.org/10.1113/EP085390 | |
dc.identifier.citation | Experimental Physiology. Hoboken, v. 101, n. 1, p. 67-80, 2016. | |
dc.identifier.doi | 10.1113/EP085390 | |
dc.identifier.issn | 0958-0670 | |
dc.identifier.uri | http://repositorio.unifesp.br/handle/11600/49659 | |
dc.identifier.wos | WOS:000368251900010 | |
dc.language.iso | eng | |
dc.publisher | Wiley-blackwell | |
dc.relation.ispartof | Experimental Physiology | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | Rostral Ventrolateral Medulla | en |
dc.subject | Circulating Angiotensin-Ii | en |
dc.subject | Nucleus-Tractus-Solitarii | en |
dc.subject | Nervous-System Activity | en |
dc.subject | Brain-Stem Preparation | en |
dc.subject | Rat Carotid-Body | en |
dc.subject | Renovascular Hypertension | en |
dc.subject | Renal Denervation | en |
dc.subject | Neurogenic Hypertension | en |
dc.subject | Goldblatt Hypertension | en |
dc.title | Sympathetic overactivity occurs before hypertension in the two-kidney, one-clip model | en |
dc.type | info:eu-repo/semantics/article |