Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/37012 http://dx.doi.org/10.1152/ajpheart.00657.2013 |
Resumo: | Neurons 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. |
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Pedrino, Gustavo R.Calderon, Alfredo S.Andrade, Mary AnnCravo, Sergio L. [UNIFESP]Toney, Glenn M.Universidade Federal de Goiás (UFG)Univ Texas Hlth Sci Ctr San AntonioUniversidade Federal de São Paulo (UNIFESP)2016-01-24T14:34:45Z2016-01-24T14:34:45Z2013-12-01American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 305, n. 12, p. H1781-H1789, 2013.0363-6135http://repositorio.unifesp.br/handle/11600/37012http://dx.doi.org/10.1152/ajpheart.00657.201310.1152/ajpheart.00657.2013WOS:000328748300011Neurons 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.National Heart, Lung, and Blood InstituteConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ Fed Goias, Dept Physiol Sci, Goiania, Go, BrazilUniv Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USAUniv Texas Hlth Sci Ctr San Antonio, Ctr Biomed Neurosci, San Antonio, TX 78229 USAUniversidade Federal de São Paulo, Dept Physiol, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Physiol, São Paulo, BrazilNational Heart, Lung, and Blood Institute: HL-102310CNPq: 477832/2010-5Web of ScienceH1781-H1789engAmer Physiological SocAmerican Journal of Physiology-heart and Circulatory Physiologyangiotensin IIhigh-salt diethypertensionrostral ventrolateral medulla vasomotor neuronssingle unit recordingsympathetic nerve activityDischarge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive ratsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/370122023-02-15 10:46:34.654metadata only accessoai:repositorio.unifesp.br:11600/37012Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-02-15T13:46:34Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
title |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
spellingShingle |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats Pedrino, Gustavo R. angiotensin II high-salt diet hypertension rostral ventrolateral medulla vasomotor neurons single unit recording sympathetic nerve activity |
title_short |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
title_full |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
title_fullStr |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
title_full_unstemmed |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
title_sort |
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats |
author |
Pedrino, Gustavo R. |
author_facet |
Pedrino, Gustavo R. Calderon, Alfredo S. Andrade, Mary Ann Cravo, Sergio L. [UNIFESP] Toney, Glenn M. |
author_role |
author |
author2 |
Calderon, Alfredo S. Andrade, Mary Ann Cravo, Sergio L. [UNIFESP] Toney, Glenn M. |
author2_role |
author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de Goiás (UFG) Univ Texas Hlth Sci Ctr San Antonio Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Pedrino, Gustavo R. Calderon, Alfredo S. Andrade, Mary Ann Cravo, Sergio L. [UNIFESP] Toney, Glenn M. |
dc.subject.eng.fl_str_mv |
angiotensin II high-salt diet hypertension rostral ventrolateral medulla vasomotor neurons single unit recording sympathetic nerve activity |
topic |
angiotensin II high-salt diet hypertension rostral ventrolateral medulla vasomotor neurons single unit recording sympathetic nerve activity |
description |
Neurons 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. |
publishDate |
2013 |
dc.date.issued.fl_str_mv |
2013-12-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:34:45Z |
dc.date.available.fl_str_mv |
2016-01-24T14:34:45Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 305, n. 12, p. H1781-H1789, 2013. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/37012 http://dx.doi.org/10.1152/ajpheart.00657.2013 |
dc.identifier.issn.none.fl_str_mv |
0363-6135 |
dc.identifier.doi.none.fl_str_mv |
10.1152/ajpheart.00657.2013 |
dc.identifier.wos.none.fl_str_mv |
WOS:000328748300011 |
identifier_str_mv |
American Journal of Physiology-heart and Circulatory Physiology. Bethesda: Amer Physiological Soc, v. 305, n. 12, p. H1781-H1789, 2013. 0363-6135 10.1152/ajpheart.00657.2013 WOS:000328748300011 |
url |
http://repositorio.unifesp.br/handle/11600/37012 http://dx.doi.org/10.1152/ajpheart.00657.2013 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
American Journal of Physiology-heart and Circulatory Physiology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
H1781-H1789 |
dc.publisher.none.fl_str_mv |
Amer Physiological Soc |
publisher.none.fl_str_mv |
Amer Physiological Soc |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764194359017472 |