Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions

Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions

Autor Johnson, Robert A. Autor UNIFESP Google Scholar
Kozma, Fruzsina Google Scholar
Colombari, Eduardo Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Semmelweis University of Medicine
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.
Palavra-chave carbon monoxide
heme
heme oxygenase
blood pressure
central nervous system
vascular tone
Idioma Inglês
Data de publicação 1999-01-01
Publicado em Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 32, n. 1, p. 1-14, 1999.
ISSN 0100-879X (Sherpa/Romeo, fator de impacto)
Publicador Associação Brasileira de Divulgação Científica
Extensão 1-14
Fonte http://dx.doi.org/10.1590/S0100-879X1999000100001
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000078324100001
SciELO S0100-879X1999000100001 (estatísticas na SciELO)
Endereço permanente http://repositorio.unifesp.br/handle/11600/717

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