Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions

Detalhes bibliográficos
Autor(a) principal: Johnson, Robert A. [UNIFESP]
Data de Publicação: 1999
Outros Autores: Kozma, Fruzsina, Colombari, Eduardo [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1590/S0100-879X1999000100001
http://repositorio.unifesp.br/handle/11600/717
Resumo: Carbon monoxide (CO) is a pollutant commonly recognized for its toxicological attributes, including CNS and cardiovascular effects. But CO is also formed endogenously in mammalian tissues. Endogenously formed CO normally arises from heme degradation in a reaction catalyzed by heme oxygenase. While inhibitors of endogenous CO production can raise arterial pressure, heme loading can enhance CO production and lead to vasodepression. Both central and peripheral tissues possess heme oxygenases and generate CO from heme, but the inability of heme substrate to cross the blood brain barrier suggests the CNS heme-heme oxygenase-CO system may be independent of the periphery. In the CNS, CO apparently acts in the nucleus tractus solitarii (NTS) promoting changes in glutamatergic neurotransmission and lowering blood pressure. At the periphery, the heme-heme oxygenase-CO system can affect cardiovascular functions in a two-fold manner; specifically: 1) heme-derived CO generated within vascular smooth muscle (VSM) can promote vasodilation, but 2) its actions on the endothelium apparently can promote vasoconstriction. Thus, it seems reasonable that the CNS-, VSM- and endothelial-dependent actions of the heme-heme oxygenase-CO system may all affect cardiac output and vascular resistance, and subsequently blood pressure.
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spelling Carbon monoxide: from toxin to endogenous modulator of cardiovascular functionscarbon monoxidehemeheme oxygenaseblood pressurecentral nervous systemvascular toneCarbon monoxide (CO) is a pollutant commonly recognized for its toxicological attributes, including CNS and cardiovascular effects. But CO is also formed endogenously in mammalian tissues. Endogenously formed CO normally arises from heme degradation in a reaction catalyzed by heme oxygenase. While inhibitors of endogenous CO production can raise arterial pressure, heme loading can enhance CO production and lead to vasodepression. Both central and peripheral tissues possess heme oxygenases and generate CO from heme, but the inability of heme substrate to cross the blood brain barrier suggests the CNS heme-heme oxygenase-CO system may be independent of the periphery. In the CNS, CO apparently acts in the nucleus tractus solitarii (NTS) promoting changes in glutamatergic neurotransmission and lowering blood pressure. At the periphery, the heme-heme oxygenase-CO system can affect cardiovascular functions in a two-fold manner; specifically: 1) heme-derived CO generated within vascular smooth muscle (VSM) can promote vasodilation, but 2) its actions on the endothelium apparently can promote vasoconstriction. Thus, it seems reasonable that the CNS-, VSM- and endothelial-dependent actions of the heme-heme oxygenase-CO system may all affect cardiac output and vascular resistance, and subsequently blood pressure.Universidade Federal de São Paulo (UNIFESP)Semmelweis University of MedicineUNIFESPSciELOAssociação Brasileira de Divulgação CientíficaUniversidade Federal de São Paulo (UNIFESP)Semmelweis University of MedicineJohnson, Robert A. [UNIFESP]Kozma, FruzsinaColombari, Eduardo [UNIFESP]2015-06-14T13:24:49Z2015-06-14T13:24:49Z1999-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion1-14application/pdfhttp://dx.doi.org/10.1590/S0100-879X1999000100001Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 32, n. 1, p. 1-14, 1999.10.1590/S0100-879X1999000100001S0100-879X1999000100001.pdf0100-879XS0100-879X1999000100001http://repositorio.unifesp.br/handle/11600/717WOS:000078324100001engBrazilian Journal of Medical and Biological Researchinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-07-29T00:41:48Zoai:repositorio.unifesp.br/:11600/717Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-07-29T00:41:48Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
title Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
spellingShingle Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
Johnson, Robert A. [UNIFESP]
carbon monoxide
heme
heme oxygenase
blood pressure
central nervous system
vascular tone
title_short Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
title_full Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
title_fullStr Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
title_full_unstemmed Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
title_sort Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
author Johnson, Robert A. [UNIFESP]
author_facet Johnson, Robert A. [UNIFESP]
Kozma, Fruzsina
Colombari, Eduardo [UNIFESP]
author_role author
author2 Kozma, Fruzsina
Colombari, Eduardo [UNIFESP]
author2_role author
author
dc.contributor.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
Semmelweis University of Medicine
dc.contributor.author.fl_str_mv Johnson, Robert A. [UNIFESP]
Kozma, Fruzsina
Colombari, Eduardo [UNIFESP]
dc.subject.por.fl_str_mv carbon monoxide
heme
heme oxygenase
blood pressure
central nervous system
vascular tone
topic carbon monoxide
heme
heme oxygenase
blood pressure
central nervous system
vascular tone
description Carbon monoxide (CO) is a pollutant commonly recognized for its toxicological attributes, including CNS and cardiovascular effects. But CO is also formed endogenously in mammalian tissues. Endogenously formed CO normally arises from heme degradation in a reaction catalyzed by heme oxygenase. While inhibitors of endogenous CO production can raise arterial pressure, heme loading can enhance CO production and lead to vasodepression. Both central and peripheral tissues possess heme oxygenases and generate CO from heme, but the inability of heme substrate to cross the blood brain barrier suggests the CNS heme-heme oxygenase-CO system may be independent of the periphery. In the CNS, CO apparently acts in the nucleus tractus solitarii (NTS) promoting changes in glutamatergic neurotransmission and lowering blood pressure. At the periphery, the heme-heme oxygenase-CO system can affect cardiovascular functions in a two-fold manner; specifically: 1) heme-derived CO generated within vascular smooth muscle (VSM) can promote vasodilation, but 2) its actions on the endothelium apparently can promote vasoconstriction. Thus, it seems reasonable that the CNS-, VSM- and endothelial-dependent actions of the heme-heme oxygenase-CO system may all affect cardiac output and vascular resistance, and subsequently blood pressure.
publishDate 1999
dc.date.none.fl_str_mv 1999-01-01
2015-06-14T13:24:49Z
2015-06-14T13:24:49Z
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/10.1590/S0100-879X1999000100001
Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 32, n. 1, p. 1-14, 1999.
10.1590/S0100-879X1999000100001
S0100-879X1999000100001.pdf
0100-879X
S0100-879X1999000100001
http://repositorio.unifesp.br/handle/11600/717
WOS:000078324100001
url http://dx.doi.org/10.1590/S0100-879X1999000100001
http://repositorio.unifesp.br/handle/11600/717
identifier_str_mv Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 32, n. 1, p. 1-14, 1999.
10.1590/S0100-879X1999000100001
S0100-879X1999000100001.pdf
0100-879X
S0100-879X1999000100001
WOS:000078324100001
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Brazilian Journal of Medical and Biological Research
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 1-14
application/pdf
dc.publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
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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