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

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dc.creatorPedrino, Gustavo Rodrigues
dc.creatorCalderon, Alfredo S.
dc.creatorAndrade, Mary Ann
dc.creatorCravo, Sergio Luiz Domingues
dc.creatorToney, Glenn M.
dc.date.accessioned2021-01-15T14:04:33Z
dc.date.available2021-01-15T14:04:33Z
dc.date.issued2013
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.pt_BR
dc.identifier.citationPEDRINO, Gustavo R. et al. Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats. American Journal of Physiology. Heart and Circulatory Physiology, Rockville, v. 305, n. 12, p. H1781-H1789, 2013.pt_BR
dc.identifier.doi10.1152/ajpheart.00657.2013
dc.identifier.issn 0363-6135
dc.identifier.issne- 1522-1539
dc.identifier.urihttp://repositorio.bc.ufg.br/handle/ri/19294
dc.language.isoengpt_BR
dc.publisher.countryEstados unidospt_BR
dc.publisher.departmentInstituto de Ciências Biológicas - ICB (RG)pt_BR
dc.rightsAcesso Abertopt_BR
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAngiotensin IIpt_BR
dc.subjectSympathetic nerve activitypt_BR
dc.subjectHigh-salt dietpt_BR
dc.subjectSingle unit recordingpt_BR
dc.subjectHypertensionpt_BR
dc.subjectRostral ventrolateral medulla vasomotor neuronspt_BR
dc.titleDischarge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive ratspt_BR
dc.typeArtigopt_BR

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