1: Braz J Med Biol Res. 1999 Jan;32(1):1-14. 

Carbon monoxide: from toxin to endogenous modulator of cardiovascular functions.

Johnson RA, Kozma F, Colombari E.

Departamento de Fisiologia, Escola Paulista de Medicina, Universidade Federal de
Sao Paulo, Brasil.

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.

Publication Types:
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    Review, Tutorial

PMID: 10347762 [PubMed - indexed for MEDLINE]