Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats

Detalhes bibliográficos
Autor(a) principal: Sato, Monica Akemi [UNIFESP]
Data de Publicação: 2001
Outros Autores: Menani, J. V., Lopes, Oswaldo Ubriaco [UNIFESP], Colombari, Eduardo [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: https://doi.org/10.1161/01.HYP.38.3.560
http://repositorio.unifesp.br/handle/11600/43899
Resumo: It has been suggested that increased sympathetic activity and arterial chemoreceptors are important for the high blood pressure in spontaneously hypertensive rats (SHR). Electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) abolish (1) the cardiovascular responses to chemoreflex activation with potassium cyanide (KCN) in normotensive rats and (2) the hypertension that follows acute aortic baroreceptor denervation in rats. Therefore, in this study we investigated the effects of electrolytic lesions of the commNTS on basal mean arterial pressure (MAP), baroreflex, and chemoreflex in SHR and in normotensive control Wistar-Kyoto (WKY) and Wistar rats. CommNTS lesions elicited a dramatic fall in MAP to normal levels during the period Of Study (from the first to fourth day following lesions) in SHR and almost no changes in WKY and Wistar rats. The pressor responses to chemoreflex activation with KCN tested in the days 1 and 4 after commNTS lesions were abolished in SHR and in normotensive strains. The reflex tachycardia induced by sodium nitroprusside was also attenuated in days 1 and 4 after commNTS lesions in SHR, WKY, and Wistar rats. The data suggest that the integrity of commNTS is important for the maintenance or high blood pressure in SHR and for the reflex responses dependent on sympathetic activation either in SHR or in normotensive strains.
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spelling Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive ratsbaroreceptorschemoreceptorssolitary nucleusrats, spontaneously hypertensiveIt has been suggested that increased sympathetic activity and arterial chemoreceptors are important for the high blood pressure in spontaneously hypertensive rats (SHR). Electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) abolish (1) the cardiovascular responses to chemoreflex activation with potassium cyanide (KCN) in normotensive rats and (2) the hypertension that follows acute aortic baroreceptor denervation in rats. Therefore, in this study we investigated the effects of electrolytic lesions of the commNTS on basal mean arterial pressure (MAP), baroreflex, and chemoreflex in SHR and in normotensive control Wistar-Kyoto (WKY) and Wistar rats. CommNTS lesions elicited a dramatic fall in MAP to normal levels during the period Of Study (from the first to fourth day following lesions) in SHR and almost no changes in WKY and Wistar rats. The pressor responses to chemoreflex activation with KCN tested in the days 1 and 4 after commNTS lesions were abolished in SHR and in normotensive strains. The reflex tachycardia induced by sodium nitroprusside was also attenuated in days 1 and 4 after commNTS lesions in SHR, WKY, and Wistar rats. The data suggest that the integrity of commNTS is important for the maintenance or high blood pressure in SHR and for the reflex responses dependent on sympathetic activation either in SHR or in normotensive strains.Univ Fed Sao Paulo, Escola Paulista Med, Dept Physiol, BR-04023060 Sao Paulo, BrazilUNESP, Fac Odontol, Dept Physiol & Pathol, Araraquara, BrazilUniv Fed Sao Paulo, Escola Paulista Med, Dept Physiol, BR-04023060 Sao Paulo, BrazilWeb of ScienceLippincott Williams & WilkinsUniversidade Federal de São Paulo (UNIFESP)UNESPSato, Monica Akemi [UNIFESP]Menani, J. V.Lopes, Oswaldo Ubriaco [UNIFESP]Colombari, Eduardo [UNIFESP]2018-06-15T17:38:28Z2018-06-15T17:38:28Z2001-09-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion560-564https://doi.org/10.1161/01.HYP.38.3.560Hypertension. Philadelphia: Lippincott Williams & Wilkins, v. 38, n. 3, p. 560-564, 2001.10.1161/01.HYP.38.3.5600194-911Xhttp://repositorio.unifesp.br/handle/11600/43899WOS:000171308400006engHypertensioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-05-02T13:44:17Zoai:repositorio.unifesp.br/:11600/43899Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-05-02T13:44:17Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
title Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
spellingShingle Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
Sato, Monica Akemi [UNIFESP]
baroreceptors
chemoreceptors
solitary nucleus
rats, spontaneously hypertensive
title_short Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
title_full Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
title_fullStr Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
title_full_unstemmed Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
title_sort Lesions of the commissural nucleus of the solitary tract reduce arterial pressure in spontaneously hypertensive rats
author Sato, Monica Akemi [UNIFESP]
author_facet Sato, Monica Akemi [UNIFESP]
Menani, J. V.
Lopes, Oswaldo Ubriaco [UNIFESP]
Colombari, Eduardo [UNIFESP]
author_role author
author2 Menani, J. V.
Lopes, Oswaldo Ubriaco [UNIFESP]
Colombari, Eduardo [UNIFESP]
author2_role author
author
author
dc.contributor.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
UNESP
dc.contributor.author.fl_str_mv Sato, Monica Akemi [UNIFESP]
Menani, J. V.
Lopes, Oswaldo Ubriaco [UNIFESP]
Colombari, Eduardo [UNIFESP]
dc.subject.por.fl_str_mv baroreceptors
chemoreceptors
solitary nucleus
rats, spontaneously hypertensive
topic baroreceptors
chemoreceptors
solitary nucleus
rats, spontaneously hypertensive
description It has been suggested that increased sympathetic activity and arterial chemoreceptors are important for the high blood pressure in spontaneously hypertensive rats (SHR). Electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) abolish (1) the cardiovascular responses to chemoreflex activation with potassium cyanide (KCN) in normotensive rats and (2) the hypertension that follows acute aortic baroreceptor denervation in rats. Therefore, in this study we investigated the effects of electrolytic lesions of the commNTS on basal mean arterial pressure (MAP), baroreflex, and chemoreflex in SHR and in normotensive control Wistar-Kyoto (WKY) and Wistar rats. CommNTS lesions elicited a dramatic fall in MAP to normal levels during the period Of Study (from the first to fourth day following lesions) in SHR and almost no changes in WKY and Wistar rats. The pressor responses to chemoreflex activation with KCN tested in the days 1 and 4 after commNTS lesions were abolished in SHR and in normotensive strains. The reflex tachycardia induced by sodium nitroprusside was also attenuated in days 1 and 4 after commNTS lesions in SHR, WKY, and Wistar rats. The data suggest that the integrity of commNTS is important for the maintenance or high blood pressure in SHR and for the reflex responses dependent on sympathetic activation either in SHR or in normotensive strains.
publishDate 2001
dc.date.none.fl_str_mv 2001-09-01
2018-06-15T17:38:28Z
2018-06-15T17:38:28Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://doi.org/10.1161/01.HYP.38.3.560
Hypertension. Philadelphia: Lippincott Williams & Wilkins, v. 38, n. 3, p. 560-564, 2001.
10.1161/01.HYP.38.3.560
0194-911X
http://repositorio.unifesp.br/handle/11600/43899
WOS:000171308400006
url https://doi.org/10.1161/01.HYP.38.3.560
http://repositorio.unifesp.br/handle/11600/43899
identifier_str_mv Hypertension. Philadelphia: Lippincott Williams & Wilkins, v. 38, n. 3, p. 560-564, 2001.
10.1161/01.HYP.38.3.560
0194-911X
WOS:000171308400006
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Hypertension
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 560-564
dc.publisher.none.fl_str_mv Lippincott Williams & Wilkins
publisher.none.fl_str_mv Lippincott Williams & Wilkins
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 biblioteca.csp@unifesp.br
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