Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats

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dc.contributor.authorPedrino, Gustavo R.
dc.contributor.authorCalderon, Alfredo S.
dc.contributor.authorAndrade, Mary Ann
dc.contributor.authorCravo, Sergio L. [UNIFESP]
dc.contributor.authorToney, Glenn M.
dc.contributor.institutionUniversidade Federal de Goiás (UFG)
dc.contributor.institutionUniv Texas Hlth Sci Ctr San Antonio
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:34:45Z
dc.date.available2016-01-24T14:34:45Z
dc.date.issued2013-12-01
dc.description.abstractNeurons of the rostral ventrolateral medulla (RVLM) are critical for generating and regulating sympathetic nerve activity (SNA). Systemic administration of ANG II combined with a high-salt diet induces hypertension that is postulated to involve elevated SNA. However, a functional role for RVLM vasomotor neurons in ANG II-salt hypertension has not been established. Here we tested the hypothesis that RVLM vasomotor neurons have exaggerated resting discharge in rats with ANG II-salt hypertension. Rats in the hypertensive (HT) group consumed a high-salt (2% NaCl) diet and received an infusion of ANG II (150 ng.kg(-1).min(-1) sc) for 14 days. Rats in the normotensive (NT) group consumed a normal salt (0.4% NaCl) diet and were infused with normal saline. Telemetric recordings in conscious rats revealed that mean arterial pressure (MAP) was significantly increased in HT compared with NT rats (P < 0.001). Under anesthesia (urethane/chloralose), MAP remained elevated in HT compared with NT rats (P < 0.01). Extracellular single unit recordings in HT (n = 28) and NT (n = 22) rats revealed that barosensitive RVLM neurons in both groups (HT, 23 cells; NT, 34 cells) had similar cardiac rhythmicity and resting discharge. However, a greater (P < 0.01) increase of MAP was needed to silence discharge of neurons in HT (17 cells, 44 +/- 5 mmHg) than in NT (28 cells, 29 +/- 3 mmHg) rats. Maximum firing rates during arterial baroreceptor unloading were similar across groups. We conclude that heightened resting discharge of sympathoexcitatory RVLM neurons is not required for maintenance of neurogenic ANG II-salt hypertension.en
dc.description.affiliationUniv Fed Goias, Dept Physiol Sci, Goiania, Go, Brazil
dc.description.affiliationUniv Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA
dc.description.affiliationUniv Texas Hlth Sci Ctr San Antonio, Ctr Biomed Neurosci, San Antonio, TX 78229 USA
dc.description.affiliationUniversidade Federal de São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipNational Heart, Lung, and Blood Institute
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIDNational Heart, Lung, and Blood Institute: HL-102310
dc.description.sponsorshipIDCNPq: 477832/2010-5
dc.format.extentH1781-H1789
dc.identifierhttp://dx.doi.org/10.1152/ajpheart.00657.2013
dc.identifier.citationAmerican Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 305, n. 12, p. H1781-H1789, 2013.
dc.identifier.doi10.1152/ajpheart.00657.2013
dc.identifier.issn0363-6135
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/37012
dc.identifier.wosWOS:000328748300011
dc.language.isoeng
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal of Physiology-heart and Circulatory Physiology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectangiotensin IIen
dc.subjecthigh-salt dieten
dc.subjecthypertensionen
dc.subjectrostral ventrolateral medulla vasomotor neuronsen
dc.subjectsingle unit recordingen
dc.subjectsympathetic nerve activityen
dc.titleDischarge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive ratsen
dc.typeinfo:eu-repo/semantics/article
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