Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions
Autor(a) principal: | |
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Data de Publicação: | 1999 |
Outros Autores: | , |
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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Repositório Institucional da UNIFESP |
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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 |
_version_ |
1814268401710792704 |