Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure
Autor(a) principal: | |
---|---|
Data de Publicação: | 2005 |
Outros Autores: | , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1152/ajpregu.00053.2005 http://repositorio.unifesp.br/handle/11600/28522 |
Resumo: | In the present study, we investigated the effects of inhibition of the caudal ventrolateral medulla (CVLM) with the GABA(A) agonist muscimol combined with the blockade of glutamatergic mechanism in the nucleus of the solitary tract (NTS) with kynurenic acid (kyn) on mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances. in male Holtzman rats anesthetized intravenously with urethane/chloralose, bilateral injections of muscimol (120 pmol) into the CVLM or bilateral injections of kyn (2.7 nmol) into the NTS alone increased MAP to 186 +/- 11 and to 142 +/- 6 mmHg, respectively, vs. control: 105 +/- 4 mmHg; HR to 407 +/- 15 and to 412 +/- 18 beats per minute (bpm), respectively, vs. control: 352 +/- 12 bpm; and renal, mesenteric and hindquarter vascular resistances. However, in rats with the CVLM bilaterally blocked by muscimol, additional injections of kyn into the NTS reduced MAP to 88 +/- 5 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Moreover, in rats with the glutamatergic mechanisms of the NTS blocked by bilateral injections of kyn, additional injections of muscimol into the CVLM also reduced MAP to 92 +/- 2 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Simultaneous blockade of NTS and CVLM did not modify the increase in HR but also abolished the increase in renal vascular resistance produced by each treatment alone. the results suggest that important pressor mechanisms arise from the NTS and CVLM to control vascular resistance and arterial pressure under the conditions of the present study. |
id |
UFSP_df31530486155855205aef72295070d6 |
---|---|
oai_identifier_str |
oai:repositorio.unifesp.br/:11600/28522 |
network_acronym_str |
UFSP |
network_name_str |
Repositório Institucional da UNIFESP |
repository_id_str |
3465 |
spelling |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressureventrolateral medullagammagamma-aminobutyric acidL-glutamatemuscimolsympathetic systemIn the present study, we investigated the effects of inhibition of the caudal ventrolateral medulla (CVLM) with the GABA(A) agonist muscimol combined with the blockade of glutamatergic mechanism in the nucleus of the solitary tract (NTS) with kynurenic acid (kyn) on mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances. in male Holtzman rats anesthetized intravenously with urethane/chloralose, bilateral injections of muscimol (120 pmol) into the CVLM or bilateral injections of kyn (2.7 nmol) into the NTS alone increased MAP to 186 +/- 11 and to 142 +/- 6 mmHg, respectively, vs. control: 105 +/- 4 mmHg; HR to 407 +/- 15 and to 412 +/- 18 beats per minute (bpm), respectively, vs. control: 352 +/- 12 bpm; and renal, mesenteric and hindquarter vascular resistances. However, in rats with the CVLM bilaterally blocked by muscimol, additional injections of kyn into the NTS reduced MAP to 88 +/- 5 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Moreover, in rats with the glutamatergic mechanisms of the NTS blocked by bilateral injections of kyn, additional injections of muscimol into the CVLM also reduced MAP to 92 +/- 2 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Simultaneous blockade of NTS and CVLM did not modify the increase in HR but also abolished the increase in renal vascular resistance produced by each treatment alone. the results suggest that important pressor mechanisms arise from the NTS and CVLM to control vascular resistance and arterial pressure under the conditions of the present study.Universidade Federal de São Paulo, Dept Physiol, EPM, São Paulo, BrazilUNESP, Fac Odontol, Dept Physiol & Pathol, Araraquara, BrazilABC, Fac Med, Dept Physiol, Santo Andre, BrazilUniversidade Federal de São Paulo, Dept Physiol, EPM, São Paulo, BrazilWeb of ScienceAmer Physiological SocUniversidade Federal de São Paulo (UNIFESP)UNESPUniversidade Federal do ABC (UFABC)Moreira, Thiago Santos [UNIFESP]Sato, Monica AkemiTakakura, Ana Carolina Thomaz [UNIFESP]Menani, Jose VanderleiColombari, Eduardo [UNIFESP]2016-01-24T12:38:07Z2016-01-24T12:38:07Z2005-11-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionR1416-R1425http://dx.doi.org/10.1152/ajpregu.00053.2005American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 289, n. 5, p. R1416-R1425, 2005.10.1152/ajpregu.00053.20050363-6119http://repositorio.unifesp.br/handle/11600/28522WOS:000232528200025engAmerican Journal of Physiology-regulatory Integrative and Comparative Physiologyinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2016-01-24T10:38:07Zoai:repositorio.unifesp.br/:11600/28522Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652016-01-24T10:38:07Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
title |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
spellingShingle |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure Moreira, Thiago Santos [UNIFESP] ventrolateral medulla gamma gamma-aminobutyric acid L-glutamate muscimol sympathetic system |
title_short |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
title_full |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
title_fullStr |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
title_full_unstemmed |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
title_sort |
Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure |
author |
Moreira, Thiago Santos [UNIFESP] |
author_facet |
Moreira, Thiago Santos [UNIFESP] Sato, Monica Akemi Takakura, Ana Carolina Thomaz [UNIFESP] Menani, Jose Vanderlei Colombari, Eduardo [UNIFESP] |
author_role |
author |
author2 |
Sato, Monica Akemi Takakura, Ana Carolina Thomaz [UNIFESP] Menani, Jose Vanderlei Colombari, Eduardo [UNIFESP] |
author2_role |
author author author author |
dc.contributor.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) UNESP Universidade Federal do ABC (UFABC) |
dc.contributor.author.fl_str_mv |
Moreira, Thiago Santos [UNIFESP] Sato, Monica Akemi Takakura, Ana Carolina Thomaz [UNIFESP] Menani, Jose Vanderlei Colombari, Eduardo [UNIFESP] |
dc.subject.por.fl_str_mv |
ventrolateral medulla gamma gamma-aminobutyric acid L-glutamate muscimol sympathetic system |
topic |
ventrolateral medulla gamma gamma-aminobutyric acid L-glutamate muscimol sympathetic system |
description |
In the present study, we investigated the effects of inhibition of the caudal ventrolateral medulla (CVLM) with the GABA(A) agonist muscimol combined with the blockade of glutamatergic mechanism in the nucleus of the solitary tract (NTS) with kynurenic acid (kyn) on mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances. in male Holtzman rats anesthetized intravenously with urethane/chloralose, bilateral injections of muscimol (120 pmol) into the CVLM or bilateral injections of kyn (2.7 nmol) into the NTS alone increased MAP to 186 +/- 11 and to 142 +/- 6 mmHg, respectively, vs. control: 105 +/- 4 mmHg; HR to 407 +/- 15 and to 412 +/- 18 beats per minute (bpm), respectively, vs. control: 352 +/- 12 bpm; and renal, mesenteric and hindquarter vascular resistances. However, in rats with the CVLM bilaterally blocked by muscimol, additional injections of kyn into the NTS reduced MAP to 88 +/- 5 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Moreover, in rats with the glutamatergic mechanisms of the NTS blocked by bilateral injections of kyn, additional injections of muscimol into the CVLM also reduced MAP to 92 +/- 2 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Simultaneous blockade of NTS and CVLM did not modify the increase in HR but also abolished the increase in renal vascular resistance produced by each treatment alone. the results suggest that important pressor mechanisms arise from the NTS and CVLM to control vascular resistance and arterial pressure under the conditions of the present study. |
publishDate |
2005 |
dc.date.none.fl_str_mv |
2005-11-01 2016-01-24T12:38:07Z 2016-01-24T12:38:07Z |
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 |
http://dx.doi.org/10.1152/ajpregu.00053.2005 American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 289, n. 5, p. R1416-R1425, 2005. 10.1152/ajpregu.00053.2005 0363-6119 http://repositorio.unifesp.br/handle/11600/28522 WOS:000232528200025 |
url |
http://dx.doi.org/10.1152/ajpregu.00053.2005 http://repositorio.unifesp.br/handle/11600/28522 |
identifier_str_mv |
American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 289, n. 5, p. R1416-R1425, 2005. 10.1152/ajpregu.00053.2005 0363-6119 WOS:000232528200025 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
American Journal of Physiology-regulatory Integrative and Comparative Physiology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
R1416-R1425 |
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 |
biblioteca.csp@unifesp.br |
_version_ |
1814268434818531328 |