Role of endogenous carbon monoxide in central regulation of arterial pressure

Detalhes bibliográficos
Autor(a) principal: Johnson, Robert A. [UNIFESP]
Data de Publicação: 1997
Outros Autores: Colombari, Eduardo [UNIFESP], Colombari, Debora Simões de Almeida [UNIFESP], Lavesa, M., Talman, W. T., Nasjletti, A.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: https://doi.org/10.1161/01.HYP.30.4.962
http://repositorio.unifesp.br/handle/11600/43847
Resumo: We investigated the contribution of neural mechanisms to the arterial pressure increase produced by zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), an inhibitor of endogenous carbon monoxide synthesis. The arterial baroreceptor reflex control of heart rate was examined in rats with and without ZnDPBG pretreatment (45 mu mol/kg IP) by analysis of the arterial pressure-heart rate relationship during infusions of phenylephrine or sodium nitroprusside to vary arterial pressure. ZnDPBG increased arterial pressure from 110+/-3 to 126+/-2 mm Hg without eliciting bradycardia. The maximum gain of the heart rate response to changes in arterial pressure was attenuated by ZnDPBG treatment (-1.9+/-0.3 versus -4.8+/-1.0 bpm/mm Hg). The possibility that ZnDPBG elevates arterial pressure by attenuating baroreceptor reflex function was addressed by comparing the presser response to ZnDPBG (45 mu mol/kg IP) in rats with and without sinoaortic denervation. The presser effect of ZnDPBG was similar in rats with and without arterial baroreceptor deafferentation, implying that the increase in pressure is nat simply the consequence of attenuated baroreceptor reflex function per se. The possibility that ZnDPBG increases arterial pressure via an effect on the nucleus tractus solitarii (NTS) also was investigated ZnDPBG (1 nmol in 100 nL) injected into the NTS of rats increased arterial pressure from 111+/-4 to 126+/-5 mm Hg, and this effect was reversed by an ipsilateral microinjection of carbon monoxide into the NTS. Accordingly, the pressor effect of ZnDPBG may rely on inhibition of carbon monoxide production in the NTS. This implies that carbon monoxide formed by brain heme oxygenase plays a role in the central regulation of arterial pressure.
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spelling Role of endogenous carbon monoxide in central regulation of arterial pressurecarbon monoxideheme oxygenaseblood pressurereflex, baroreceptorsolitary tract nucleushypertensionWe investigated the contribution of neural mechanisms to the arterial pressure increase produced by zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), an inhibitor of endogenous carbon monoxide synthesis. The arterial baroreceptor reflex control of heart rate was examined in rats with and without ZnDPBG pretreatment (45 mu mol/kg IP) by analysis of the arterial pressure-heart rate relationship during infusions of phenylephrine or sodium nitroprusside to vary arterial pressure. ZnDPBG increased arterial pressure from 110+/-3 to 126+/-2 mm Hg without eliciting bradycardia. The maximum gain of the heart rate response to changes in arterial pressure was attenuated by ZnDPBG treatment (-1.9+/-0.3 versus -4.8+/-1.0 bpm/mm Hg). The possibility that ZnDPBG elevates arterial pressure by attenuating baroreceptor reflex function was addressed by comparing the presser response to ZnDPBG (45 mu mol/kg IP) in rats with and without sinoaortic denervation. The presser effect of ZnDPBG was similar in rats with and without arterial baroreceptor deafferentation, implying that the increase in pressure is nat simply the consequence of attenuated baroreceptor reflex function per se. The possibility that ZnDPBG increases arterial pressure via an effect on the nucleus tractus solitarii (NTS) also was investigated ZnDPBG (1 nmol in 100 nL) injected into the NTS of rats increased arterial pressure from 111+/-4 to 126+/-5 mm Hg, and this effect was reversed by an ipsilateral microinjection of carbon monoxide into the NTS. Accordingly, the pressor effect of ZnDPBG may rely on inhibition of carbon monoxide production in the NTS. This implies that carbon monoxide formed by brain heme oxygenase plays a role in the central regulation of arterial pressure.UNIFESP,EPM,DEPT PHYSIOL,SAO PAULO,BRAZILUNIV IOWA,DEPT NEUROL,IOWA CITY,IA 52242VET ADM MED CTR,IOWA CITY,IAUNIFESP,EPM,DEPT PHYSIOL,SAO PAULO,BRAZILWeb of ScienceAmer Heart AssocUniversidade Federal de São Paulo (UNIFESP)UNIV IOWAVET ADM MED CTRJohnson, Robert A. [UNIFESP]Colombari, Eduardo [UNIFESP]Colombari, Debora Simões de Almeida [UNIFESP]Lavesa, M.Talman, W. T.Nasjletti, A.2018-06-15T17:35:15Z2018-06-15T17:35:15Z1997-10-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion962-967https://doi.org/10.1161/01.HYP.30.4.962Hypertension. Dallas: Amer Heart Assoc, v. 30, n. 4, p. 962-967, 1997.10.1161/01.HYP.30.4.9620194-911Xhttp://repositorio.unifesp.br/handle/11600/43847WOS:A1997YC80200031engHypertensioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-05-02T15:52:32Zoai:repositorio.unifesp.br/:11600/43847Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-05-02T15:52:32Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Role of endogenous carbon monoxide in central regulation of arterial pressure
title Role of endogenous carbon monoxide in central regulation of arterial pressure
spellingShingle Role of endogenous carbon monoxide in central regulation of arterial pressure
Johnson, Robert A. [UNIFESP]
carbon monoxide
heme oxygenase
blood pressure
reflex, baroreceptor
solitary tract nucleus
hypertension
title_short Role of endogenous carbon monoxide in central regulation of arterial pressure
title_full Role of endogenous carbon monoxide in central regulation of arterial pressure
title_fullStr Role of endogenous carbon monoxide in central regulation of arterial pressure
title_full_unstemmed Role of endogenous carbon monoxide in central regulation of arterial pressure
title_sort Role of endogenous carbon monoxide in central regulation of arterial pressure
author Johnson, Robert A. [UNIFESP]
author_facet Johnson, Robert A. [UNIFESP]
Colombari, Eduardo [UNIFESP]
Colombari, Debora Simões de Almeida [UNIFESP]
Lavesa, M.
Talman, W. T.
Nasjletti, A.
author_role author
author2 Colombari, Eduardo [UNIFESP]
Colombari, Debora Simões de Almeida [UNIFESP]
Lavesa, M.
Talman, W. T.
Nasjletti, A.
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
UNIV IOWA
VET ADM MED CTR
dc.contributor.author.fl_str_mv Johnson, Robert A. [UNIFESP]
Colombari, Eduardo [UNIFESP]
Colombari, Debora Simões de Almeida [UNIFESP]
Lavesa, M.
Talman, W. T.
Nasjletti, A.
dc.subject.por.fl_str_mv carbon monoxide
heme oxygenase
blood pressure
reflex, baroreceptor
solitary tract nucleus
hypertension
topic carbon monoxide
heme oxygenase
blood pressure
reflex, baroreceptor
solitary tract nucleus
hypertension
description We investigated the contribution of neural mechanisms to the arterial pressure increase produced by zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG), an inhibitor of endogenous carbon monoxide synthesis. The arterial baroreceptor reflex control of heart rate was examined in rats with and without ZnDPBG pretreatment (45 mu mol/kg IP) by analysis of the arterial pressure-heart rate relationship during infusions of phenylephrine or sodium nitroprusside to vary arterial pressure. ZnDPBG increased arterial pressure from 110+/-3 to 126+/-2 mm Hg without eliciting bradycardia. The maximum gain of the heart rate response to changes in arterial pressure was attenuated by ZnDPBG treatment (-1.9+/-0.3 versus -4.8+/-1.0 bpm/mm Hg). The possibility that ZnDPBG elevates arterial pressure by attenuating baroreceptor reflex function was addressed by comparing the presser response to ZnDPBG (45 mu mol/kg IP) in rats with and without sinoaortic denervation. The presser effect of ZnDPBG was similar in rats with and without arterial baroreceptor deafferentation, implying that the increase in pressure is nat simply the consequence of attenuated baroreceptor reflex function per se. The possibility that ZnDPBG increases arterial pressure via an effect on the nucleus tractus solitarii (NTS) also was investigated ZnDPBG (1 nmol in 100 nL) injected into the NTS of rats increased arterial pressure from 111+/-4 to 126+/-5 mm Hg, and this effect was reversed by an ipsilateral microinjection of carbon monoxide into the NTS. Accordingly, the pressor effect of ZnDPBG may rely on inhibition of carbon monoxide production in the NTS. This implies that carbon monoxide formed by brain heme oxygenase plays a role in the central regulation of arterial pressure.
publishDate 1997
dc.date.none.fl_str_mv 1997-10-01
2018-06-15T17:35:15Z
2018-06-15T17:35:15Z
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.30.4.962
Hypertension. Dallas: Amer Heart Assoc, v. 30, n. 4, p. 962-967, 1997.
10.1161/01.HYP.30.4.962
0194-911X
http://repositorio.unifesp.br/handle/11600/43847
WOS:A1997YC80200031
url https://doi.org/10.1161/01.HYP.30.4.962
http://repositorio.unifesp.br/handle/11600/43847
identifier_str_mv Hypertension. Dallas: Amer Heart Assoc, v. 30, n. 4, p. 962-967, 1997.
10.1161/01.HYP.30.4.962
0194-911X
WOS:A1997YC80200031
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 962-967
dc.publisher.none.fl_str_mv Amer Heart Assoc
publisher.none.fl_str_mv Amer Heart Assoc
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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