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Chronic depression of hypothalamic paraventricular neuronal activity produces sustained hypotension in hypertensive rats

2014Journal article Open access
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dc.contributor.authorGeraldes, Vera
dc.contributor.authorGonçalves-Rosa, Nataniel
dc.contributor.authorLiu, Beihui
dc.contributor.authorPaton, Julian F. R.
dc.contributor.authorRocha, Isabel
dc.date.accessioned2020-07-22T10:06:42Z
dc.date.available2020-07-22T10:06:42Z
dc.date.issued2014
dc.description© 2013 The Authors. Experimental Physiology © 2013 The Physiological Society.pt_PT
dc.description.abstractChanges in the sympathetic nervous system are responsible for the initiation, development and maintenance of hypertension. An important central sympathoexcitatory region is the paraventricular nucleus (PVN) of the hypothalamus, which may become more active in hypertensive conditions, as shown in acute studies previously. Our objective was to depress PVN neuronal activity chronically by the overexpression of an inwardly rectifying potassium channel (hKir2.1), while evaluating the consequences on blood pressure (BP) and its reflex regulation. In spontaneously hypertensive rats (SHRs) and Wistar rats (WKY) lentiviral vectors (LVV-hKir2.1; LV-TREtight-Kir-cIRES-GFP5 4 × 10(9) IU and LV-Syn-Eff-G4BS-Syn-Tetoff 6.2 × 10(9) IU in a ratio 1:4) were stereotaxically microinjected bilaterally into the PVN. Sham-treated SHRs and WKY received bilateral PVN microinjections of LVV-eGFP (LV-Syn-Eff-G4BS-Syn-Tetoff 6.2 × 10(9) IU and LV-TREtight-GFP 5.7 × 10(9) IU in a ratio 1:4). Blood pressure was monitored continuously by radio-telemetry and evaluated over 75 days. Baroreflex gain was evaluated using phenylephrine (25 μg ml(-1), i.v.), whereas lobeline (25 μg ml(-1), i.v.) was used to stimulate peripheral chemoreceptors. In SHRs but not normotensive WKY rats, LVV-hKir2.1 expression in the PVN produced time-dependent and significant decreases in systolic (from 158 ± 3 to 132 ± 6 mmHg; P < 0.05) and diastolic BP (from 135 ± 4 to 113 ± 5 mmHg; P < 0.05). The systolic BP low-frequency band was reduced (from 0.79 ± 0.13 to 0.42 ± 0.09 mmHg(2); P < 0.05), suggesting reduced sympathetic vasomotor tone. Baroreflex gain was increased and peripheral chemoreflex depressed after PVN microinjection of LVV-hKir2.1. We conclude that the PVN plays a major role in long-term control of BP and sympathetic nervous system activity in SHRs. This is associated with reductions in both peripheral chemosensitivity and respiratory-induced sympathetic modulation and an improvement in baroreflex sensitivity. Our results support the PVN as a powerful site to control BP in neurogenic hypertension.pt_PT
dc.description.sponsorshipThis work was suported by Fundacão para a Ciência e Tecnologia – PTDC/SAU-OSM/109081/2008, British Heart Foundation and NIH.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationExperimental Physiology, 99: 89-100pt_PT
dc.identifier.doi10.1113/expphysiol.2013.074823pt_PT
dc.identifier.eissn1469-445X
dc.identifier.issn0958-0670
dc.identifier.urihttp://hdl.handle.net/10451/44108
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherJohn Wiley & Sons, Inc.pt_PT
dc.relation.publisherversionhttps://physoc.onlinelibrary.wiley.com/journal/1469445Xpt_PT
dc.titleChronic depression of hypothalamic paraventricular neuronal activity produces sustained hypotension in hypertensive ratspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FSAU-OSM%2F109081%2F2008/PT
oaire.citation.endPage100pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage89pt_PT
oaire.citation.titleExperimental Physiologypt_PT
oaire.citation.volume99pt_PT
oaire.fundingStream3599-PPCDT
person.familyNameGeraldes
person.familyNameGoncalves Rosa
person.familyNamerocha
person.givenNameVera
person.givenNameNataniel
person.givenNameisabel
person.identifier.ciencia-idD51D-E96C-1633
person.identifier.ciencia-id7313-0C25-7377
person.identifier.orcid0000-0003-1275-3459
person.identifier.orcid0000-0001-5571-8616
person.identifier.orcid0000-0002-7582-0893
person.identifier.ridM-4137-2013
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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relation.isAuthorOfPublication33f7ff12-f5ac-408c-954e-773d371a9e12
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relation.isAuthorOfPublication.latestForDiscovery33f7ff12-f5ac-408c-954e-773d371a9e12
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